LECTURES  ON  THE 
HEART 


BY  THE  SAME  AUTHOR 

THE  MECHANISM  OF  THE 
HEAET  BEAT. 

With    Especial    Eeference    to 
its   Clinical  Pathology    .      .      .   $7.00  NET 

CLINICAL  DISORDERS  OF 
THE  HEART  BEAT. 

A  Handbook   for   Practition- 
ers   and    Students     ....     2.00 

CLINICAL 

ELECTROCARDIOGRAPHY      2.00 

HEART.  A  Journal  for  the 
Study  of  the  Circulation. 
Edited  by  Thomas  Lewis. 

Per  Volume 5.00      " 

PAUL  B.  HOEBER 

67-69   East   59th   Street,   New   York 


LECTURES  ON  THE 
HEAET 


COMPRISING  THE  HERTER  LECTURES,    (BALTIMORE)  ; 
A  HARVEY  LECTURE,    (NEW  YORK) 

AND  AN  ADDRESS  TO  THE  FACULTY  OF  MEDICINE 
AT  McGILL  UNIVERSITY,    (MONTREAL). 


BY 

THOMAS  LEWIS,  M.D.,  F.R.C.P.,  D.Sc. 

Physician  City  of  London  Hospital,  Assistant  Physician  and 

Lecturer  in   Cardiac  Pathology,   University 

College  Hospital,  London. 


NEW  YORK 

PAUL  B.  HOEBER 

1915 


Copyright,  1915 
Bv  PAUL  B.  HOEBER 


Published  March,  1915 


Printed  in  the  U.  S.  A. 


QPi 

L67 


PREFACE 

The  five  lectures  comprising  this  book  were  delivered 
during  a  brief  visit  to  the  American  continent  in  the 
Autumn  of  1914. 

The  Herter  lectures  were  written  to  emphasise  the 
advantages  of  intimately  combining  clinical  and  labora- 
tory observations.  Co-operation  between  wards  and 
laboratories,  as  my  visit  has  clearly  taught  me,  is  no- 
where more  freely  or  widely  cultivated  than  in  the  Medi- 
cal Schools  of  America.  To  these  lectures,  the  Harvey 
lecture,  which  deals  with  questions  of  physiological  in- 
terest, seems  a  fitting  introduction.  The  address  at  Mon- 
treal serves  to  illustrate  in  a  more  extended  manner  the 
application  of  laboratory  methods  to  questions  of  imme- 
diate and  practical  consequence. 

It  is  a  pleasure  to  acknowledge  my  indebtedness  to  the 
Committee  of  the  Herter  Foundation,  and  to  the  Harvey 
Society,  who  have  kindly  sanctioned  the  publication  of 
the  lectures  in  this  form. 

THOMAS  LEWIS. 

November  3rd,  1914. 


6346 


CONTENTS. 


PAGE 
CHAPTER  I. 

THE  EXCITATION  WAVE  IN  THE  HEART  "         . .          . .         . .         . .  3 

A  lecture  delivered  before  the  Harvey  Society,  New  York, 
October  25th,  1914. 


The  three  Eerier  Lectures  upon  "  Clinical  Medicine  and  Laboratory 
Methods  "  delivered  at  the  25th  Anniversary  of  the  Johns  Hop- 
kins Hospital,  Baltimore,  October  6th,  8th  and  9th,  1914- 


CHAPTER  II 
LECTURE  1.     THE  METHOD  OF  ELECTROCARDIOGRAPHY  EXEMPLIFIED        35 

CHAPTER  III 

LECTURE  2.     "THE  RELATION  OF  AURICULAR    SYSTOLE  TO  HEART 

SOUNDS  AND  MURMURS  "     . .          . .          . .         . .         . .         53 

CHAPTER  IV 

LECTURE  3.     "  OBSERVATIONS  UPON  DYSPNCEA,  WITH  ESPECIAL  REF- 
ERENCE TO  ACIDOSIS  "  . .          . .          •  •          •  •         81 


CHAPTER  V 

OBSERVATTONS  UPON  CARDIAC  SYNCOPE  "         . .          . .         . .         . .         99 

Delivered  at  the  opening  of  the  Faculty  of  Medicine,  McGill 
University,  Montreal,  October  5th,  1914- 


HAEVEY  LECTURE 

ON 

"  THE  EXCITATION  WAVE  IN  THE  HEAKT " 
DELIVERED  BEFORE   THE  HARVEY  SOCIETY, 
YORK,  OCTOBER,  25TH,  1914. 


CHAPTER  I 
*  THE  EXCITATION  WAVE  IN  THE  HEART 

Mr.  President  and  Gentlemen, 

May  I  preface  what  I  have  to  say  to-day  by  telling  you  how 
much  I  appreciate  your  invitation  to  deliver  this  Harvey  lec- 
ture. How  clearly  the  great  physician,  with  whose  name  this 
Society  associates  itself,  to  whose  name  it  delights  to  do  honour, 
saw  that  the  natural  and  safe  advance  of  Medicine  should  follow 
its  advance  guard,  physiology.  Has  he  not  fitly  been  named  the 
Father  of  that  Science  ?  Is  it  not  a  matter  of  profound  satisfac- 
tion and  pride  to  us  that  this  pioneer  of  experimental  physi- 
ology should  have  been  of  our  profession  and  that  his  greatest 
discovery  should  have  been  prompted  by  observations  upon  the 
human  being  ?  As  Harvey  by  physiological  study  laid  the 
foundation  of  Medicine  as  an  exact  science,  so  to-day,  if  we 
have  learned  the  lesson  which  his  writings  should  teach  us,  we 
shall  maintain  this  tradition,  preserving  the  closest  intimacy 
between  our  conceptions  of  the  physiology  and  pathology  of  man- 
kind. 

If  we  as  students  of  the  heart  are  exponents  of  such  new 
methods  as  clinical  electrocardiography,  should  we  not  in  aspir- 
ing to  become  the  humble  disciples  of  this  great  teacher,  first 
probe  the  normal  phenomena  of  the  heart's  electric  forces  to  the 
utmost  ?  Can  we  who  are  met  to  emphasise  the  name  and  works 
of  this  man,  for  all  time  the  first  exponent  of  the  heart's  mechan- 
ism and  function,  more  fittingly  employ  ourselves  than  by 
earnestly  considering  the  natural  heart  beat?  Gentlemen,  in 
these  questions  you  will  find  my  reason  for  attempting  to  ex- 


4  Chapter  I 

plain  to  you  the  origin  and  course  of  the  natural  excitation  wave. 
Harvey  our  master  chose  as  his  illustration  the  heart  of  a  King's 
deer ;  we  his  disciples  may  select  a  less  regal  beast,  the  dog. 

General  principles. 

That  the  heart  beat  is  accompanied  by  an  electric  discharge 
was  first  clearly  shown  by  Kolliker  and  Miiller  in  1856.  These 
workers  laid  upon  the  beating  ventricle  the  nerve  of  a  nerve 
muscle  preparation,  and  noticed  that  at  each  contraction  of  the 
ventricle  the  nerve  became  excited.  In  that  simple  yet  ingeni- 
ous experiment  our  knowledge  of  the  excitatory  process  com- 
mences. Since  that  time,,  a  great  number-  of  workers  have 
examined  the  mammalian  ventricle  from  the  point  of  view  of  the 
electric  currents  found  in  it.  It  will  not  be  possible  in  this 
address  to  do  justice  to  them,  for  the  last  chapters  of  the  story 
are  in  themselves  of  undue  length.  I  do  not  propose  therefore 
to  treat  these  questions  historically,  but  to  describe  to  you  in 
language  as  simple  as  possible  the  results  of  recent  observation. 
For  some  five  years  my  laboratory  has  been  engaged  in  the 
study  of  this  question,  and  I  have  been  joined  in  the  work  by  a 
number  of  collaborators.  These  collaborators  have  been,  for 
the  most  part,  your  countrymen,  and  it  is  a  lively  pleasure  to 
me  to  know  that  several  of  them  are  here  to-night.  The  Drs. 
Oppenheimer  of  this  city  published  with  me  one  of  our  first 
papers.  Dr.  Meakins  of  Montreal  and  Dr.  White  of  Boston 
joined  in  these  researches  at  a  later  date;  and  most  recently  I 
have  had  the  help  of  Dr.  Rothschild  of  Mt.  Sinai  Hospital. 

Let  us  in  the  first  place  examine  the  electric  events  which 
are  associated  with  the  contraction  of  a  simple  strip  of  muscle, 
and  formulate  the  general  laws  which  are  to  guide  us  in  our 
examination  of  so  complex  a  structure  as  the  heart.  If  we 
connect  a  simple  strip  of  muscle,  (P-D,  Fig.  1)  by  means  of 
non-polarisable  electrodes  to  a  sensitive  galvanometer,  and  stim- 
ulate one  end  of  this  muscle  (P),  the  galvanometer  exhibits 


The  Excitation  Wave  in  the  Heart 


two   deflections.     The  meaning   of   these   deflections,   together 
forming  when  recorded  a  diphasic  curve,  is  known.     The  first 
deflection   accompanies  the  commencement  of  muscle  activity 
in  the  neighbourhood  of  P  (Fig.  1ft)?  and  this  deflection  has 
the  same  direction  as  has  the  deflection  obtained  when  the  zinc 
terminal  of  a  copper-zinc  couple  replaces  the  active  muscle  P. 
When  muscle  is  active,  therefore,  it  is  in  a  state  of  relative 
negativity,  in  precisely  the  same 
sense  that  the  zinc  of-a  battery 
is     relatively     negative.     This 
negativity  and  the  passage  of  a 
current  from  the  inactive  point 
through  the  galvanometer  to  the 
active  point,  produces  the  first 
swing  of  the  string  recorder,  a 
swing  which  is  upright  in  our 
curves.     It  is  a  large  swing  be- 
cause it  is  unbalanced;  the  re- 
gion   of    the   other    contact    re- 
maining for  the  time  inactive. 
The  second  deflection  of  which  I 
have  spoken  is  due  to  similar 
conditions;  it  is  produced  after 
the    excitatory    process,    associ- 
ated with  the  contraction,   has 
travelled  in   a  wave  from  the 
proximal  (P)  to  the  distal  end 
(D)  of  the  muscle  strip.     D  is  active  while  at  P  activity  has 
subsided  (Fig.  Id).     The  portion  of  the  muscle  which  has  the 
electric  charge  of  similar  kind  to  our  zinc  terminal  becomes 
transferred  as  the  wave  of  activity  passes  from  P  to  D.     Con- 
sequently after  the  active  process  reaches  D  the  swing  of  the 
galvanometer  is  reversed ;  a  current  passes  from  P  through  the 
galvanometer  to  D,  and  develops  the  second  deflection  which  is 


Fig.  1.  A  diagram,  illustrating 
the  development  and  subsid- 
ence of  activity  (and  negativ- 
ity) in  a  single  muscle  strip, 
responding  to  a  stimulus  ap- 
plied at  P.  The  correspond- 
ing and  successive  phases  of 
the  galvanometric  curve  are 
shown  in  the  four  lines  a,  b, 
c  and  d. 


6 


Chapter  I 


of  opposite  direction  to  the  first.  Thus  the  two  phases  of  our 
recorded  curve  are  due  to  a  change  in  the  relation  of  the  active 
point  to  the  two  leading  off  contacts,  and  this  change  produces 
a  reversal  of  direction,  the  two  deflections  together  comprising 
a  diphasic  effect.  The  culmination  of  the  first  phase  can  be 
shown  theoretically  and  experimentally  to  coincide  with  the  ar- 
rival of  the  excitatory  process  at  the  distal  end,  in  short  strips 
of  muscle  (Fig.  16).  For  when  this  occurs  a  balance  begins 
to  be  established  between  the  electric  state  under  the  two  con- 
tacts. Evidently  when  the  first  phase  is  complete  and  the  curve 
is  about  to  cross  the  base  line,  activity  is  exactly  equal  under 
the  contacts  (Fig.  Ic).  Now  this  is  a  simple  experiment  and 
easily  understood,  once  it  is  recognised  that  electrically  active 
muscle  is  relatively  negative  to  inactive  muscle.  Simple  as  it 
is,  it  is  fundamental  to  electrocardiograph^ ;  the  whole  of  our 

interpretations  are  ulti- 
mately based  upon  it. 

It  leads  us  immedi- 
ately to  our  second  law, 
which  tells  us  that  the 
direction  which  the  ex- 
citation wave  takes, 
governs  the  form  of  the 
resulting  curve.  And 
when  I  speak  of  excita- 
tion wave,  you  should 
recollect  that  this  wave 
is  intimately  bound  up 
with  the  contraction 
wave;  it  precedes  it  by 
an  extremely  short  in- 
terval, and  is  presum- 
ably the  result  of  those  physico-chemical  processes  which  at 
any  point  immediately  precede  actual  contraction.  That  the 


LLL 


II 


Pig.  2.  A  similar  diagram,  illustrating  the 
inversion  of  the  curve  when  the  order 
of  contraction  is  reversed,  and  its  isopo- 
tentiality  when  the  ends  of  the  strip 
are  activated  simultaneously.  The  di- 
rections in  which  contraction  is  driven 
are  indicated  by  the  arrows. 


The  Excitation  Wave  in  the  Heart  7 

shape  of  our  curve  is  governed  by  the  direction  of  the  wave  is 
readily  shown  by  our  simple  strip  of  muscle,  for  let  us  reverse 
the  direction  of  contraction  by  stimulating  the  originally  distal 
end  (D),  and  forcing  the  wave  to  travel  from  D  to  P.  We 
still  obtain  a  diphasic  curve;  but 

compared  with  our  first  curve,  each       

phase  is  now  reversed  in  direction       < T 

(Fig.  2a  and  c)  ;  it  is  easy  to  see 
why  this  is  so,  for  having  reversed 
the  contraction,  we  have  reversed  I  I  I 


the  order  in  which  the  ends  of  the 
strip  become  relatively  negative. 
But  supposing  that  the  same  strip  is 
stimulated  at  its  centre  point  (Fig. 

F.-I  x  j    ,1         ,T  ,.  Fig.  3.     A    similar    diagram: 

26),  and  that  the  contraction  wave         6  to    show   that   maximal 
travels  with  equal  rapidity  to  the  excursion  of  the  galvano- 

metric     recorder     is     ob- 
two  ends,  where  our  contacts  are  ar-  tained  when  the  interval 


ranged       "Fach     pnrl     thpn     hpomnpcs  of  dela^  between  the  ar' 

mgea.     j!,ac  rival    of   the    excitation 

negative  at  the  same  instant  and  the  wave  at  the  contacts  is 

two   effects   neutralise   each   other. 

In  these  circumstances  there  will  be  no  swing  of  the  recording 
instrument.  Further,  supposing  that  the  excitation  wave  is 
started  now  at  P  and  then  at  a  series  of  regularly  placed  points 
up  to  a  centre  point  (Fig.  3),  then  a  graduated  series  of  curves 
will  be  obtained,  from  a  simple  and  large  diphasic  curve  at  one 
end  of  the  scale,  through  curves  of  gradually  diminishing  ampli- 
tude, to  a  horizontal  line  at  the  other.  From  observations  of 
this  kind  it  is  clear  that  the  amplitude  of  the  first  phase  is 
greatest  when  the  time  interval  between  the  receipt  of  the  exci- 
tation at  the  two  contacts  is  greatest.  If  the  time  interval  is 
nothing,  a  state  of  isopotentiality  is  established,  and  as  the  time 
interval  is  longer  and  longer,  so  the  effects  are  more  and  more 
unbalanced,  and  the  culmination,  occurring  later  and  later,  has 
more  and  more  opportunity  to  develope.  When  we  deal  with  a 


8 


Chapter  I 


sheet  of  muscle,  for  example  the  auricle,  as  opposed  to  a  strip, 
then  the  same  statement  applies  ;  if  a  point  is  stimulated  on  the 

surface  and  a  pair  of  contacts  is  ar- 
ranged at  a  little  distance  away,  then 
the  amplitude  is  greatest  when  the 
contacts  are  radial  *  to  the  point  of 
stimulation  (Fig.  4a)  for  with  these 
conditions  the  interval  between  the 
arrival  of  the  wave  at  the  two  con- 
tacts is  maximal. 

In  these  observations  we  have  the 

stnts™6  shirt  6of  "ZE     basis  of  °™  fl^  investigations  of  the 

cle,  excited  at  a,  b  or     mammalian  heart. 

c,  and  examined  at  two 

central    contact    points. 

The     excursion     of    the  QF  ElXCITATION 

recorder       is       greatest 

when    the    contacts    are  WAVE    IN    THE   AURICLE. 

in  the  line  of  the  exci- 

tation wave;  i.e.,  when     T]w        ^  w^fe  ^  relatively  nega- 

the     muscle     is     stimu-  L 

lated  at  a;  it  is  least  tive  io  all  outlying  ones. 

when  stimulation  is  at 

Ln"  ttiX  TU  SI         H  ™  Place  a  P«r  of  contacts  upon 
multaneously  developed     a  given  area  of  the  mammalian  auricle 

at  the  contacts.  ,  ,,  .,  ,  ,         - 

and  rotate  them  through  an  angle  of 

90  degrees,  our  curve  varies  in  amplitude.  We  are  able  quickly 
to  isolate  a  line  which  yields  the  greatest  amplitude  when  the 
contacts  are  placed  along  it.  Such  lines  are  favourable  lines 
from  which  to  lead,  and  we  may  conclude  that  such  lines 
approximately  represent  the  lines  along  which  the  natural  ex- 
citation wave  travels.  Such  lines  in  the  mammalian  auricle 
converge  to  a  point  in  the  neighbourhood  of  the  angle  of  supe- 
rior vena  cava  and  right  appendix,  where  as  you  know  the  chief 
part  of  the  sino-auricular  node  is  situate.  A  specially  favour- 
able line  is  that  of  the  ta?nia  terminalis.  We  have,  therefore, 


*  As  Engelmann  has  shown  the  excitation  wave  radiates  from  a  point  of 
stimulation. 


The  Excitation  Wave  in  the  Heart  9 

a  preliminary  evidence  that  the  excitation  wave  radiates  from 
a  central  position,  the  region  of  the  angle  named. 

We  take  our  second  step.  If  the  natural  excitation  wave 
spreads  along  radiating  lines  from  the  upper  regions  of  the 
sulcus  terminalis  and  we  place  one  contact  over  this  region  and 
the  other  upon  a  circle  of  points  surrounding  it,  we  should, 
according  to  a  rule  which  has  been  formulated,,  obtain  a  series 
of  curves  of  good  excursion,  and,  if  activity  is  always  devel- 
oped under  the  central  contact  first,  this  contact  should  always 
be  primarily  negative  to  all  other  points.  That  is  to  say,  if  we 


VENA   CAVA 


tf puun . VE in     r vj  ,        <  v^C4 ^?¥^AR 


1WTERCAVAL+ 
REGIOM 


Rr  APR. 


INFERIOR     +00  **          '    l/J+«'-AUR.WAll. 

VENA   CAYA 

AUR.WAUL 

Fig.  5.  A  diagram,  illustrating  a  method  of  examining  a  sheet  of  muscle. 
A  central  contact  lies  over  the  region  giving  rise  to  the  excitation 
wave,  the  second  contact  is  placed  at  outlying  points  successively. 
In  these  circumstances,  the  central  contact  always  exhibits  primary 
negativity. 

make  such  radiating  leads,  maintaining  our  central  contact 
upon  the  point  at  which  the  excitation  wave  arises,  a  series  of 
curves  should  be  obtained,  of  which  the  first  phases  are  always 
of  a  given  sign;  the  direction  of  the  deflections  should  always 
indicate  primary  negativity  of  the  central  point  (Fig.  5),  i.e., 
the  first  deflections  should  aM  be  upright. 

There  is  but  one  portion  of  the  superficies  of  the  mammalian 
auricle  which  exhibits  these  electric  relations  during  normal 
contractions.  If  one  contact  is  placed  on  the  upper  reaches  of 
the  sulcus  terminalis  and  the  other  contact  is  moved  along  a 


10 


Chapter  I 


SVC. 


circumference  surrounding  this  centre,  it  matters  not  where 
this  second  contact  lies,  the  first  deflection  obtained  with  auric- 
ular systole  is  upward  in  direction,  indicating  relative  nega- 
tivity of  the  centre  point.  Such  are  the  events  when  the  centre 

contact  lies  in  ap- 
position to  the 
head  and  superfi- 
cial part  of  the 
s  i  n  o  -  auricular 
node  (Fig.  6). 
Now  this  experi- 
ment is  a  striking 


l.V.C. 


one,  for  the  auric- 


Fig.  6.  The  contacts  as  applied  to  an  auricle. 
The  central  contact,  which  is  invariably  rela- 
tively negative  to  outlying  points  when  activ- 
ity in  the  auricle  starts,  overlies  the  8. A. 
node. 


ular  muscle  in  this 
neighbourhood  i  s 
thin,  and  the  8-A 
node  lies  in  what 
we  may  regard  as 
the  centre  of  a 
muscle  sheet,  that 
is  to  say,  a  com- 
plete circle  of  points  may  be  arranged  around  it.  There  is 
little  or  no  possibility  that  this  region  of  the  heart  receives  the 
excitation  wave  from  some  deeper  structure,  for  all  possible 
paths  to  the  node  may 'be  investigated.  The  conclusion  that 
this  centre  is  the  centre  in  which  the  excitation  wave  originates 
is  most  strongly  suggested.  The  observations  upon  which  this 
proposition  rests  were  made  by  Wybauw  and  by  observation  in 
my  laboratory  in  conjunction  with  the  Drs.  Oppenheimer. 
They  are  observations  which  I  have  repeatedly  confirmed  since 
our  original  publication,  and  which  have  been  recently  con- 
firmed by  Eyster  and  Meek,  independent  workers  in  this  land. 
In  the  pig's  heart,  the  sino-auricular  node  lies  further  up  the 
sulcus  than  in  the  dog,  and  in  one  animal  of  this  species  I  have 


The  Excitation  Wave  in  the  Heart 


11 


found  the  point  of  relative  negativity  to  be  in  a  corresponding 
position.  It  lay,  as  Ivy  Mackenzie  subsequently  snowed  his- 
tologically,  immediately  over  the  sino-auricular  node  in  this 
particular  animal,  as  it  had  lain  in  all  our  dogs. 

Forcing  a  natural  excitation  wave. 

There  is  a  second  and  distinct  method  of  approaching  the 
same  subject.  Suppose  that  we  start  contractions  from  various 
regions  of  the  auricle  and  observe  the  type  of  curve  which  each 


i 


Fig.  7.  Three  electrocardiograms  from  a  dog  (Lead  II).  The  last  two 
cycles  in  each  curve  are  natural  heart  beats.  The  remaining  cycles  are 
in  response  to  stimulation  over  (1)  the  upper  part  of  the  sulcus  ter- 
minalis,  (2)  left  appendix,  and  (3)  inferior  cava.  The  natural  beats 
are  simulated  when  stimulation  is  in  the  region  of  the  S.A.  node. 

yields,  using  a  given  and  fixed  lead,  and  compare  such  curves 
with  those  of  the  normal  heart  beat.  I  have  said  that  the  shape 
of  the  curves  will  be  controlled  by  the  direction  which  the  ex- 


12  Chapter  I 

citation  wave  takes  in  the  muscle.  If,  as  we  stimulate  the 
auricle  to  contract,  we  discover  some  region  of  it  which  yields 
curves  which  are  identical  with  the  normal,  we  may  be  sure  that 
the  natural  excitation  waves  and  those  propagated  from  stimu- 
lation of  the  area  in  question  follow  similar  paths.  They  can 
only  follow  similar  paths  if  the  region  which  we  stimulate  is 
the  region  from  which  the  normal  excitation  waves  are  propa- 
gated. In  the  case  of  the  mammalian  auricle,  as  I  have  shown, 
there  is  but  a  single  area  which  answers  to  these  conditions 
(Fig.  7).  It  is  the  area  immediately  surrounding  the  upper 
reaches  of  the  sulcus  terminalis,  the  region  which  contains  the 
S-A  node.  Our  second  evidence,  therefore,  accords  with  our 
first;  both  indicate  the  S-A  nodal  region  as  that  in  which  the 
excitation  wave  has  its  birth. 

Extrinsic  and  intrinsic  deflections. 

I  pass  to  a  consideration  of  what  are  termed  "  outlying 
leads,"  that  is  to  say,  leads  in  which  neither  contact  lies  over 
the  S-A  node.  In  leading  directly  from  the  heart  muscle,  the 
chief  deflections  are  produced  by  the  arrival  of  the  excitatory 
process  immediately  beneath  the  contacts.  The  contacts  are 
exposed  to  the  full  force  of  this  electric  discharge.  Such  leads 
.are  very  different  from  those  utilised  in  human  electrocardio- 
graphy,  for  in  them  the  contacts  are  upon  the  limbs  and  not 
upon  the  heart.  Curves  of  the  excitation  wave  may  be  obtained 
under  each  condition,  and  for  purposes  both  of  description  and 
of  investigation,  the  direct  and  indirect  effects  should  not  be 
confused.  Especially  is  this  the  case  in  leading  from  the  heart 
itself.  In  such  leads,  the  contacts  lie  on  the  muscle  and  the 
deflections  are  of  two  kinds. 

1.  There  are  deflections  which  result  from  the  arrival  of  the 
excitation  process  immediately  beneath  the  contacts;  these  we 
term  intrinsic  deflections.  They  are  deflections,  as  you  may 


The  Excitation  Wave  in  the  Heart  13 

suppose,  which  represent  considerable  electrical  potentials  and 
have  considerable  amplitudes. 

2.  There  are  also  deflections  which  are  yielded  by  the  ex- 
citation wave,  travelling  in  distant  areas  of  the  muscle.  To 
these  we  apply  the  term  "  extrinsic  deflections/' 

A  simple  example  of  intrinsic  and  extrinsic  deflections  is  the 
following.  Let  us  place  two  contacts  upon  the  sulcus  termi- 
nalis;  at  each  beat  of  the  auricle  a  large  intrinsic  deflection  is 


m  Hi 


Fig.  8.  Simultaneous  electrocardiograms.  The  upper  curves  from  the  ap- 
pendix, the  lower  curves  from  lead  //.  Showing  the  effect  of  crushing 
the  base  of  the  appendix  and  rendering  the  tissue  under  the  contacts 
inactive.  The  chief  or  intrinsic  deflection  (Tn)  is  abolished;  the  ex- 
trinsic deflection  (Esc)  remains,  as  do  the  ventricular  deflections  (v). 

produced  by  the  arrival  of  the  excitation  wave  beneath  the 
nearest  contact.  When  the  ventricle  contracts,  the  same  con- 
tacts pick  up  smaller  electric  discharges  from  the  last  named 
chamber.  These  extrinsic  effects  are  records  of  muscle  activity 
at  a  distance.  But  the  same  double  effect  is  noticed  in  the 
auricle  itself.  If  we  lead  by  two  contacts  from  the  right 
auricular  appendix  for  example,  we  obtain  a  curve  of  the  form 
shown  in  Fig.  8  a.  You  see  the  usual  tall  spike,  but  it  is  pre- 


14  Chapter  I 

ceded  by  a  small  downward  deflection.  That  this  initial  de- 
flection is  not  produced  by  activity  in  the  appendix,  and  that 
the  chief  deflection  is,  can  readily  be  demonstrated  by  crushing 
the  base  of  the  appendix.  In  this  manner  the  appendix  is 
rendered  inactive,  and  when  this  is  accomplished,  the  type  of 
curve  changes.  The  extrinsic  effect,  the  small  initial  deflec- 
tion, remains,  while  the  intrinsic  effects  disappear  (Fig.  8&). 
Now  this  is  a  fundamental  demonstration,  for  it  permits  us 
to  analyse  those  curves  which  are  obtained  from  outlying  leads. 
All  such  leads  give  curves  of  composite  form;  consisting 
of  a  main  deflection,  which  corresponds  to  the  arrival  of  the 
excitation  process  beneath  the  contacts,  and  diminutive  initial 
deflections  which  are  due  to  the  passage  of  other  portions  of  the 
auricular  muscle  into  the  excitatory  state.  In  considering  the 
course  of  the  excitation  wave,  as  opposed  to  its  origin,  we  shall 
focus  our  attention  upon  these  chief  or  intrinsic  deflections,  for 
they  will  alone  concern  us. 

The  point  of  primary  negativity. 

It  has  been  said  that  a  single  point  of  the  auricular  muscle 
shows  negativity  relative  to  surrounding  areas  when  the  auricle 
first  becomes  active,  and  it  has  been  concluded  that  this  is  so 
because  this  area  first  developes  negativity  or  activity.  Re- 
cently we  have  been  able  to  demonstrate  (Lewis,  Meakins  and 
White)  that  such  is  indeed  the  case  by  a  direct  and  most  con- 
clusive method.  We  take  simultaneous  electrocardiograms 
(Fig.  9),  either  from  two  direct  leads  or  preferably  from  a  di- 
rect lead  and  a  standard  limb-lead  (Lead  II).  By  using  exact 
methods  of  mensuration  we  have  been  able  to  reduce  our  cus- 
tomary error  below  a  thousandth  of  a  second  and  to  measure 
the  time  of  onset  of  the  excitation  wave,  relative  to  P  in  the 
standard,  in  various  regions  of  the  auricle  with  great  accuracy. 
Having  searched  the  whole  of  the  superficies  of  both  auricles 
and  the  septum  internally  in  a  large  number  of  animals,  we  can 


The  Excitation  Wave  in  the  Heart 


15 


11 


fa* 

O    CD 


16  Chapter  I 

affirm  that  the  first  appearance  of  the  excitation  wave  is  over  the 
head  of  the  sino-auricular  node  and  that  it  appears  at  later 
times  in  all  other  regions. 

The  same  observations  provide  this  and  another  important 
evidence  that  the  S-A  nodal  region  originates  the  excitation 
wave.  It  is  the  only  region  of  the  auricle  from  which  curves 
are  obtained,,  in  which  there  are  no  initial  deflections  (Fig. 
9a)  ;  the  reason  being  that  when  the  intrinsic  deflection  is 
obtained  from  this  lead,  the  whole  of  the  rest  of  the  auricular 
tissue  is  in  a  state  of  inactivity ;  while  in  all  outlying  leads  the 
intrinsic  deflection,  which  represents  activity,  is  preceded  by 
initial  movements  of  the  string  (Fig.  9&  and  c),  which  repre- 
sent currents  from  the  preceding  activity  of  the  S-A  nodal  re- 
gion and  surrounding  areas. 

I  may  sum  up  this  the  first  part  of  my  address  to  you,  in 
the  statement  that  we  have  abundant  and  conclusive  evidence 
that  the  excitation  wave  commences  in  the  immediate  neigh- 
bourhood of  the  head  of  the  sino-auricular  node. 

II.    THE  COURSE.  OF  THE  EXCITATION  WAVE  IN  THE  AURICLE. 

When  we  examine  the  intrinsic  deflections  in  curves  from 
outlying  leads,  if  the  contacts  are  arranged  radially  to  the  S-A 
node,  the  direction  of  the  intrinsic  deflection  is  always  the  same, 
indicating  that  of  the  two  contacts  the  proximal  always  receives 
the  excitation  wave  first  (Fig.  10)  ;  we  have  taken  many  hun- 
dreds of  such  curves  without  noting  a  single  exception  to  this 
rule.  From  the  direction  of  the  intrinsic  deflection  alone  we 
may  conclude  that  the  excitation  wave  spreads  from  the  S-A 
node  in  all  directions  radially,  that  it  runs  down  the  tsenia 
terminalis  into  the  tip  of  the  .right  appendix,  along  the  intra- 
auricular  band  to  the  tip  of  the  left  appendix,  and  down  the 
septum ;  that  it  runs  into  all  the  veins,  ca.valy  coronary  and  pul- 
monary, against  the  blood  stream. 

And  these  conclusions  are  completely  substantiated  by  our 


The  Excitation  Wave  in  the  Heart  17 

readings  of  the  times  at  which  the  excitation  wave  reaches  par- 
ticular points.     If  a  series  of  contacts  is  placed  upon  the  auricle 

s.v.c 


RTPULH.VEIN  4- 


4-  LFT  PULM  VEIN 


RT  APP. 


RT  AUR.V/ALL. 


Fig.  10. 


A  diagram  illustrating  a  system  of  "  outlying  "  leads.  A  pair  of 
contacts  is  arranged  radially  to  the  node  in  various  regions.  The 
proximal  contact  always  receives  the  excitation  wave  first,  as  shown 
by  the  direction  of  the  intrinsic  deflection. 

in  a  direction  radial  to  the  8-A  node,  and  the  times  at  which 
the  excitatory  process  arrives  in  each  is  estimated  (Fig.  11  and 

SUPERIOR    CAVA   OT  SULCUS^r  INFERIOR  CAVA. 


3.        8.       7.        6.        5.       -4.        3-       2  .         I. 

Fig.  11.  A  diagram  illustrating  leads  from  serial  contacts.  If  the  S.A. 
node  lies  at  one  end  of  the  series,  the  tijne  at  which  the  excitation 
wave  appears  recedes  uniformly  throughout  the  series,  starting  at  the 
nodal  end. 

13),  a  contact  proximal  to  the  S-A  node  is  always  found  to 
receive  the  excitation  wave  before  a  point  more  distal  ;  and  if 
the  contacts  are  equidistant  from  each  other,  the  times  at  which 
the  excitation  wave  appears  at  the  individual  contacts  of  the 
series  increase  in  a  regular  order.  The  excitation  wave  passes 
up  the  superior  vena  cava  and  flows  along  it  to  a  point  well 
outside  the  pericardium  (Fig.  15)  ;  it  ends  where  the  heart 
muscle  ends  and  the  venous  muscle  begins.  It  passes  down  the 


18 


Chapter  I 


Fig.  12.  Outline  of  an  auricle  in  an  actual  experiment;  showing  the  ar- 
rangement of  the  muscle  bands;  the  concentration  point  (C.P.)  ;  and 
the  outline  of  the  8. A  node.  The  diagram  is  accurately  to  scale,  and 
illustrates  the  method  of  leading  off  by  paired  contacts  and  the  sub- 
sequent orientation. 


Fig.  13.  A  scale  drawing  from  an  actual  experiment;  showing  a  number  of 
contacts  used  for  leads  from  sulcus  and  inferior  cava.  Examples  of 
the  curves  are  shown  in  Fig.  14. 


The  Excitation  Wave  in  the  Heart 


19 


inferior  cava  to  the  edge  of  the  cuff  of  muscle  which  is  in  places 
intrapericardial,  in  places  extrapericardial  (Figs.  13  and  15). 
Knowing  the  distances  between  our  contacts  and  the  S-A 
node,  we  are  able  to  estimate  the  rates  of  conduction  of  the  wave 
to  all  parts  of  the  auricle.  The  average  transmission  times, 
distances  and  rates  are  given  in  the  accompanying  table.  The 


Region. 

Distance 
in  mm. 

Transmission 
Time. 

Transmission 
Rate. 

Number  of 
Observations. 

Intercaval    

15.2 

.0139 

1232 

18 

Intra  aur. 

Band 

12.9 

.0126 

1252 

6 

s.  v.  c  

8.2 

.0136 

588 

11 

Septum 

(mid  and  low)  . 

31.5 

.0305 

1059 

11 

Rt.    app  

28.0 

.0314 

955 

11 

Rt.  aur  

16.0 

.0206 

859 

7 

R.  Pulm.  V  

24.0 

.0254 

1121 

4 

I    V    C 

31.5 

.0325 

998 

18 

Cor.  Sinus  

43.9 

.0412 

1096 

5 

L.  Pulm.  V  

45.2 

.0412 

1118 

5 

L.  App  

44.6 

.0446 

996 

7 

Average  heart  rate  158.4. 


transmission  rates  are  wonderfully  uniform  from  node  to  all 
parts  of  the  auricle;  such  differences  as  occur  are  readily  ac- 
counted for  by  small  errors  of  measurement,  or  by  the  arrange- 
ment of  the  muscle  bands^  for  it  seems  as  if  the  rate  of  trans- 
mission is  greatest  where  the  muscle  bands  are  straight.  The 
solitary  exception  to  the  statement  that  the  rate  of  transmission 
is  uniform  and  approaches  1000  mm.  per  second  is  found  in 
the  superior  cava;  here  it  is  lower  and  we  are  inclined  to  at- 
tribute this  difference  to  the  direction  of  the  muscle  fibres  in 
this  vein ;  they  are  arranged  for  the  most  part  obliquely  across 
the  vein,  while  our  transmission  rates  have  ;been  estimated  up 
and  down  it.  We  are  unable  to  obtain  evidence  of  hindrance  to 
the  passage  of  the  wave  from  node  to  auricle  at  any  point ;  the 


20 


Chapter  I 


^> 

S2 

*  ^^ 

^ 
£ 

^ 


OS05 


Fig.   14. 


Fig.  15. 


Fig.  14.  A  diagram  showing  outlines  of  the  curves  obtained  from  5  of  the 
leads  of  Fig.  13.  Charted  in  relation  to  the  first  appearance  of  the 
excitation  wave  in  the  auricle  (8.A.N.  line).  The  intrinsic  deflection 
gradually  recedes  in  time  as  the  lead  is  taken  lower  on  the  vein, 
until  the  edge  of  the  muscle  is  reached;  the  intrinsic  deflection  is  then 
lost. 

Fig.  15.  Serial  leads  from  sulcus  and  superior  cava  in  another  auricle. 
The  times  at  which  the  excitation  wave  appeared  at  the  several  contact 
points  are  given.  From  the  highest  S.V.C.  (contacts  marked*)  no  in- 
trinsic deflections  were  obtained. 


The  Excitation  Wave  in  the  Heart 


21 


rate  of  travel  appears  to  be  uniform,  the  direction  of  travel 
radial  in  all  directions.  Neither  can  we  find  any  evidence  of 
an  increased  rate  of  conduction  to  the  A-V  node,  our  calculated 
rates  are  the  same  for  all  parts  of  the  auricular  septum  as  for 
the  rest  of  the  auricular  tissue.  We  have  also  used  special 
methods  of  estimating  the  transmission  time  from  node  to  node, 
by  a  method  which  I  do  not  propose  to  consider  in  detail,  and 
find  it  to  be  long. 

The  excitation  wave  in  the  auricle  may  be  likened  to  the 
spread  of  a  fluid 
poured  upon  a  flat 
surface,  its  edge  ad- 
vances as  an  ever 
widening  circle,  until 
the  whole  surface  is 
covered  (Fig.  16)  ; 
such  variation  as  ex- 
ists in  the  rate  of 
travel  along  various 
lines  in  the  auricle  is 
fully  accounted  for 
by  the  simple  ana- 
tomical arrangement 
of  the  tissue.  If 
we  examine  the  ar- 
rangement of  the  muscle  bands  of  any  mammalian  auricle,  we 
shall  agree,  I  think,  that  they  are  ordered  upon  a  definite  plan. 
Immediately  below  the  8-A  node  the  fibres  collect  from  all  parts 
of  the  superficies  of  the  right  auricle  in  a  curious  fan  shaped 
manner,  to  join  in  a  knot  of  tissue  which  we  term  the  concen- 
tration point  (Fig.  12  C.  P.).  The  S-A  node  is  placed  in  the 
most  advantageous  position  possible  for  a  quick  distribution  of 
the  contraction  wave  to  all  parts  of  the  auricle,  the  fibres  stream 
into  this  region  of  the  heart  from  all  the  chief  outlying  regions. 


Fig.  16.  A  diagram,  illustrating  the  spread  of 
the  excitation  wave  over  the  surface  of  the 
right  auricle.  The  spread  is  almost  uni- 
form and  follows  the  chief  muscle  bands. 


22  Chapter  I 

The  chief  fibres  of  the  right  appendix  run  direct  to  the  head 
of  the  sulcus;  the  tsenia  runs  from  bottom  to  top  of  sulcus; 
the  intra-auricular  band  runs  from  the  angle  across  to  the  left 
appendix ;  other  fibres  run  down  the  intra-auricular  septum. 

To  sum  up ;  the  excitation  wave,  which  has  its  origin  in  the 
S-A  node  spreads  immediately  and  at  rates  ranging  about 
1000  mm.  per  second  along  the  chief  muscle  tracts  which  radi- 
ate from  the  neighbourhood  of  this  node;  it  courses  throughout 
the  whole  of  the  auricular  tissue,  up  to  its  ending  upon  the 
chief  veins,  and  courses  down  the  septum  at  a  similar  speed 
to  reach  the  A-V  node,  whence  it  is  transmitted  to  the  ven- 
tricle. Is  it  not  true  to  say  that  one  auricle  contracts  before 
the  other ;  the  excitation  wave  appears  in  some  portions  of  the 
right  auricle  before  some  portions  of  the  left  and  vice-versa. 
The  spread  may  be  likened  to  the  spread  of  fluid  poured  upon 
an  almost  flat  surface. 

III.    THE    EXCITATION    WAVE    IN    THE    VENTRICLE. 

We  have  followed  the  course  of  the  excitation  wave  from  the 
sino-auricular  node,  throughout  the  auricle  and  to  the  auriculo- 
ventricular  node.  I  do  not  propose  to  deal  with  the  evidence 
for  the  transmission  of  the  impulse  from  auricle  to  ventricle. 
We  know  as  a  result  of  recent  investigations  that  it  passes 
through  the  auriculo-ventricular  bundle;  and  there  is  powerful 
evidence  that  it  is  distributed  in  the  ventricle  through  that  in- 
tricate and  almost  universal  subendocardial  network,  the  Pur- 
kin  je  system. 

We  pass  to  a  study  of  the  excitation  process  in  the  ventricle 
itself.  In  discussing  this  subject  I  propose  to  take  a  somewhat 
unusual  course.  At  a  somewhat  later  date  it  is  proposed  to 
publish  a  full  paper  on  this  subject;  the  work  of  Dr.  Roths- 
child and  myself  is  still  in  progress  but  is  sufficiently  advanced 
to  bring  before  you  in  the  form  of  a  preliminary  communica- 
tion. 


The  Excitation  Wave  in  the  Heart  23 

Our  observations  have  been  conducted  along  lines  similar  to 
those  for  the  investigation  of  the  auricle.* 

We  estimate  the  time  of  the  appearance  of  the  excitation 
wave,  relative  to  R  in  a  standard  electrocardiogram,  in  the 
various  areas  of  the  musculature.  The  problems  are  more 
difficult  than  those  connected  with  the  auricle.  In  the  last 
named  chamber,  as  we  have  seen,  the  wave  spreads  in  uniform 
and  diverging  lines.  At  an  early  stage  of  our  observations  we 
found  that  the  spread  in  the  ventricle  happens  in  an  entirely 
different  fashion.  If  we  examine  a  series  of  points  upon  a 
superficial  band  of  ventricular  muscle,  for  example,  the  con- 
spicuous fibres  which  sweep  from  the  conus  across  the  upper 
part  of  the  interventricular  groove  and  around  the  left  border 
of  the  heart  to  the  apex,,  we  immediately  ascertain  that  the 
wave  does  not  course  along  these  bands. 

Fig.  18  serves  as  an  illustration:  the  excitation  wave  appears 
at  a  series  of  points  along  the  right  border  of  this  diagram  at 
time  intervals,  .0241,  .0231,  .0198,  .0150,  .0146,  .0187  and 
.0196  sec.  after  R.  It  appears  almost  simultaneously  at  all 
these  points,  although  they  overlie  the  same  muscle  band.  We 
have  conclusive  evidence  that  the  excitatory  process  takes  little 
or  no  consideration  of  the  anatomical  arrangement  of  the  mus- 
culature of  the  ventricle.  If  we  cover  the  front  of  the  heart 
with  contacts  and  estimate  the  order  of  the  excitation  process, 
we  constantly  discover  an  area  in  the  region  of  the  anterior 
attachment  of  the  wall  of  the  right  ventricle  (shaded  area  in 
Fig.  18)  in  which  the  excitatory  process  first  commences  so 
far  as  the  superficies  of  the  heart  are  concerned.  But  there  is 
this  remarkable  fact;  there  exists  in  this  region  a  consid- 
erable area,  though  it  is  of  variable  extent,  in  which  the  ex- 
citatory process  commences  almost  simultaneously.  If  we 
examine  the  underlying  structures  we  shall  find  that  this 

*  With  the  exception  that  single  contacts  are  placed  on  the  ventricle  while 
the  second  contact  lies  on  the  chest  wall. 


24 


Chapter  I 


regon 
of  the 


is    the   most    directly    supplied    by    the    right    branch 
A-V  bundle,  and  we  have  little  doubt  that  the  distribu- 


tion  of  the  right  branch  to  this  region  is  responsible,  in  part  at 
least,  for  its  early  and  simultaneous  excitation.  Examining 
the  whole  superficial  surface  of  the  heart  in  a  number  of  ani- 


The  Excitation  Wave  in  the  Heart  25 

mals,  we  find  a  close  resemblance  in  the  distribution  from  beast 
to  beast.  The  superficial  area  which  passes  earliest  into  a 
state  of  excitation  is  almost  always  that  which  I  have 
indicated,  namely  the  portions  of  the  conus  where  these  join 
the  interventricular  groove.  This  is  the  portion  of  the  wall 
overlying*  the  large  anterior  papillary  muscle  of  the  right  ven- 
tricle. The  rest  of  the^ngbt  ventricle  becomes  active  later; 
the  latest  region  is  the  upper  wall  of  the  conus  directly  below 
the  pulmonary  valves ;  the  base  of  the  right  ventricle  at  its 
fusion  with  the  fat  in  the  A-V  groove,  and  that  portion  which 
lies  along  the  posterior  interventricular  groove,  is  almost  but 
not  quite  so  late. 

Yet  although  there  is  this  almost  constant  order,  the  time 
differences  between  the  onsets  of  activity  in  the  several  parts 
of  the  right  ventricle  are  remarkably  small.  In  the  case  of  the 
auricle,  the  wave  takes  from  start  to  finish  4  to  5,  hundredths 
of  a  second  to  complete  its  course.  In  the  ventricles,  although 
these  chambers  are  so  much  larger,  the  whole  course  is  usually 
completed  in  dogs  of  the  same  size  in  less  than  3  hundredths 
of  a  second. 

The  order  in  the  left  ventricle  is  equally  definite,  though  at 
present  I  shall  not  enter  into  detail.  The  earliest  point  is 
the  vortex  of  the  left  ventricle  or  the  extreme  apex,  and  this 
region  sometimes  successfully  rivals  the  right  ventricle  in  the 
race;  a  hundredth  of  a  second  later  the  neighbouring  points  are 
activated.  The  appearance  of  activity  over  the  remainder  of 
this  chamber  is  practically  simultaneous,  the  time  differences 
are  usually  to  be  measured  in  a  few  thousandths  of  a  second. 
The  basal  attachment  is  generally  speaking  latest  of  all  and 
practically  coincident  with  the  activity  in  the  conus  region. 

No  system  of  spread  from  point  to  point  of  the  muscle  fibres 
in  a  definite  order  can  be  imagined  which  will  explain  this 
distribution.  We  are  forced  to  assume  that  the  ventricular 
wall  is  reached  bv  an  impulse  travelling  along  a  large  number 


26 


Chapter  I 


of  paths  of  distribution.  These  paths  as  we  are  able  to  show 
are  the  Purkinje  paths.  If  we  examine  a  series  of  points, 
such  as  those  shown  in  Fig.  19  before  and  after  section  of  the 
right  branch  of  the  A-V  bundle  we  find  clear  evidence  for  this 

statement.  After  section  of  this 
branch,  as  you  are  aware,  a  con- 
spicuous change  occurs  in  the  form 
of  the  axial  electrocardiogram; 
this  change  interferes  to  some  ex- 
tent with  our  absolute  standard  of 
measurement,  but  we  are  able  to 
ascertain  the  relative  order  before 
and  after  the  interference  Avith 
precision.  It  is  found  that  prior 
to  section  the  right  A^entricle  be- 
comes active  before  the  left  in 
such  a  series  of  contacts  as  is  fig- 
ured ;  but  after  section  the  order 
changes.  The  relation  of  points 
to  each  other  over  the  left  A^entricle 
remains  unaltered ;  Avhile  activity 
in  the  right  ventricle  is  materially 
delayed  and  progresses  from  left 
towards  right.  The  Purkinje  f 

over  the  right,  whereas  be-       system    is    thus    prOATed    to    be    COn-I 
fore  section  the  excitation 
wave   appeared   earliest   in 
this    region,    after    section 
it  appeared  latest. 

haATe  still  to  explain  a  great  deal. 

Even  where  we  take  into  account  this  branching  system,  we  can- 
not fully  explain  the  time  relations  over  certain  regions  unless 
Ave  assume  that  ventricular  conduction  is  much  more  rapid  than 
conduction  in  the  auricle.  To  take  an  example:  there  are  no 
free  branching  strands  to  the  region  of  the  conus ;  the  subendo- 
cardial  network  in  this  region  is  spread  as  a  continuous  sheet ; 


Fig.  19.  Outline  of  the  front 
of  a  dog's  heart,  upon 
which  five  contact  points 
were  investigated,  before 
(top  figures)  and  after 
(bottom  figures)  section 
of  the  right  branch  of  the 
A-V  bundle.  It  will  be 
noted  that  over  the  left 
ventricle  the  order  re- 
mains unchanged;  but 


cerned   in   the   distribution.     But' 
allowing  this  to  be  the   case,   w^e 


The  Excitation  Wave  in  the  Heart  27 

yet  conduction  to  the  muscle  beneath  the  pulmonary  valves  is 
extremely  rapid.  To  meet  these  difficulties  of  explanation  we 
have  devised  special  experiments.  It  has  been  necessary  to 
measure  the  rate  of  conduction  through  various  tissue  areas 
when  an  artificial  excitation  wave  is  propagated  across  contacts 
in  line  with  each  other.  The  natural  rate  of  conduction  in  the 
auricle  is  fairly  uniform  and  at  about  1000  mm.  for  a  second. 
The  rate  of  conduction  in  the  ventricle  varies  with  the  region 
examined.  It  is  highest  and  approaches  or  surpasses  2000 
mm.  per  second  where  the  muscle  is  thinnest.  It  is  lowest  and 
approaches  400  mm.  per  second  where  the  muscle  is  thickest. 
The  reason  for  this  variation  is  clear  to  us.  The  rate  of  con- 
duction through  ventricular  muscle  is  slow,  the  rate  of  conduc- 
tion through  Purkinje  substance  is  approximately  at  least  5 
times  as  fast.  When  we  excite  the  pericardial  surface,  the 
difference  in  the  times  at  which  the  excitation  wave  reaches  the 
contacts  in  line  with  the  stimulation  point,  depends  upon 
whether  the  excitation  wave  has  time  to  travel  through  and  into 
the  Purkinje  substance  and  along  it  and  out  again  through  the 
muscle  to  our  contacts,  before  it  passes  directly  to  our  contacts 
through  the  muscle  alone.  Evidently  the  thicker  the  tested 
muscle,  the  less  likelihood  is  there  of  quick  penetration.  That 
this  explanation  is  valid  is  clearly  shown  by  two  further  experi- 
ments. 

If  two  contacts  are  placed  opposite  to  each  other,  one  on  the 
pericardial,  the  other  upon  the  endocardial  surface,  the  natural 
excitation  wave  always  reaches  the  internal  contact  first  (Fig. 
20).  It  also  reaches  the  internal  contact  first,  and  by  precisely 
the  natural  time  interval,  when  an  excitation  wave  is  pro- 
voiced  from  the  outside,  provided  that  the  point  of  stimulation 
is  sufficiently  far  removed.  Thus  in  Fig.  20  e  represents  an 
external  and  i  an  internal  contact,  and  the  epicardium  is  stim- 
ulated 10  mm.  away.  The  excitation  wave  appears  at  the  in- 
ternal contact  first  and  at  the  external  contact  after  the  natural 


Chapter  I 


Fig.  20.  Two  contacts  (e  —  external,  i 
—  internal)  are  placed  on  the  epi- 
cardium  and  endocardium  respect- 
ively, and  the  heart  wall  is  stimu- 
lated at  8,  10  mm.  away.  The  exci- 
tation appears  at  the  internal  con- 
tact first  and  at  a  natural  interval, 
before  it  appears  at  the  external 
contact ;  it  travels  therefore  by  way 
of  the  Pur  kin  je  substance. 


interval.  It  has  travelled 
therefore  along  the  path 
a  a  a,  through  8  mm.  of 
muscle  and  10  mm.  of  the 
Purkinje  system  before  it 
has  travelled  through  10 
mm.  of  muscle  (path  &). 
Thus  it  prefers  to  pass 
through  10  mm.  of  Purk- 
inje substance,  rather 
than  through  2  mm.  or 
less  of  muscle. 

The   second  experiment 
is  similar  in  kind.      Two 

contacts  are  placed  on  the  right  ventricle  (Fig.  21)  and  the 
heart  is  stimulated  at  a  point  in  the  neighbourhood  of  the  sep- 
tum (n),  some  10  or  15  mm.  away.  The  interval  between  the 
arrival  of  the  excita- 
tion process  at  p  and 
d  is  relatively  long. 
(The  path  taken  is 
along  c. )  But  if  the 
point  of  stimulation 
is  moved  30  to  40 
mm.  away  (/)  and 
the  experiment  is  re- 
peated, the  interval 
is  materially  re- 
duced; in  a  number 
of  such  experiments 
it  is  reduced  until  it 
reaches  the  interval 
displayed  %  the  nat- 
ural heart  beat.  In 


Fig.  21.  A  diagram  of  the  ventricles,  seen  in 
vertical  section.  Two  contacts,  p  and  d, 
are  placed  on  the  right  ventricle.  The 
ventricle  is  stimulated  at  n  and  the  ex- 
citation wave  passes  along  the  path  c. 
The  ventricle  is  stimulated  at  /  and  the 
excitation  wave  now  appears  at  p  and  d  at 
such  times  as  to  suggest  that  it  travels 
through  Purkinje  tissue  and  bundle 
branches  a,  a,  in  preference  to  the  shorter 
course  6,  b. 


The  Excitation  Wave  in  the  Heart  29 

such  instances  the  quicker  though  far  longer  path  is  over  the 
septum  and  through  the  main  divisions  of  the  bundle  (a  a  as  op- 
posed to  &  &).  Let  us  sum  up  our  findings.  The  spread  of 
the  excitation  wave  in  the  ventricle  is  controlled  by  the  Purk- 
inje  system;  it  is  hastened  by  the  early  branching  of  this  sys- 
tem, especially  in  the  left  ventricle.  The  Purkinje  system  has 
a  high  rate  of  conduction  as  compared  to  ventricular  muscle, 
and  this  quality  also  favours  quick  distribution. 

Evidently,  before  we  may  end  our  search,  we  have  to  inves- 
tigate the  endocardial  surface  of  the  heart;  this  presents 
difficulties,  but  is  in  the  course  of  completion.  The  excitation 
wave  appears  early  inside  the  ventricle,  and  the  time  intervals 

appear  to  be  very  small ^v,; 

between  different  endo-      < < — • — > > 

cardial     regions.       We 

i    -,.  ,,         ,,  ,.  Fig.  22.     A  diagram  illustrating  the  spread 

believe  that  the  earliest  b  of  the   excitation  wave   in  the  auricle 

region  of  all  is  the  up-  from  a  central  node-    The  spread  is 

along  the  muscle  bands. 

per  part  01  the  septum 

on  the  left  side,  and  that  other  regions  become  active  according 
to  their  distance  from  the  main  distributing  tracts ;  but  this 
has  not  been  convincingly  proved.  Why  then  does  the  front 
of  the  right  ventricle  become  active  so  long  before  super- 
ficial regions  of  the  ventricle  overlying  the  left  papillary 
muscles  ?  For  a  simple  reason,  namely,  because  the  muscle 
is  thinner.  We  have  data  of  a  very  suggestive  kind  which 
appear  to  show  that,  as  Purkinje  conduction  is  extremely  rapid, 
the  excitation  process  starts  almost  simultaneously  over  the 
whole  interior  of  both  ventricles,  and  that  the  appearance  of 
activity  upon  the  superficies,  while  partially  controlled  by  the 
distance  from  the  main  Purkinje  strand,  is  chiefly  controlled 
by  the  thickness  of  the  muscle  overlying  the  Purkinje  sub- 
stance. It  is  chiefly  to  this  cause  that  we  attribute  the  early 
appearance  of  the  excitation  wave  over  the  front  of  the  right 
ventricle,  near  its  attachment,  and  at  the  vortex  of  the  left 


30 


Chapter  I 


ventricle ;  for  these  are  the  thinnest  points  of  the  ventricular 
walls.  According  to  our  view  the  excitation  spreads  in  the  ven- 
tricle along  the  Purkinje  system,  and,  appears  on  the  surface 
by  directly  piercing  the  whole  thickness  of  the  wall  (see  Fig. 
23)  ;  this  piercing  of  the  wall  is  aided  by  the  penetration  of  the 
wall  by  isolated  strands  of  the  end  arborisation  of  the  Purkinje 
system. 


Fig.  23.  The  spread  in  the  ventricle  as  it  is  conceived.  The  spread  is 
from  p,  through  branches  of  the  Purkinje  system ;  subsequently  the 
spread  is  along  the  endocardial  network  and  from  this  at  right  angles 
through  the  ventricular  wall. 

The  observations  which  I  have  briefly  surveyed  will,  I  trust, 
take  us  far  towards  a  final  explanation  of  the  normal  electro.- 
cardiogram,  for  we  are  now  in  a  position  to  state  the  regions 
which  are  excited  when  given  deflections  of  the  normal  curve 
are  inscribed;  but  this  subject  I  shall  defer.  Our  view  of  the 
distribution  in  the  ventricle  also  helps  us,  so  we  believe,  to 
understand  the  curious  alterations  of  electrocardiograms  met 
with  in  the  hypertrophies ;  for  a  thickened  left  ventricle  should 
delay  the  activity  of  the  apical  musculature,  and  by  delaying 
penetration  should  deepen  and  prolong  S  in  axial  leads.  How- 
ever, this  view  is  at  present  in  the  stage  of  tentative  hypothesis. 

Finally,  a  word  on  conduction  rates  in  various  regions  of 
the  heart.  We  find  the  conduction  rate  to  increase  as  we  pass 
from :  — 


The  Excitation  Wave  in  the  Heart  31 

1.  Ventricular  muscle  to 

2.  Auricular  muscle  to 

3.  Purkinje  substance. 

It  is  to  be  remarked  that  the  glycogen  content  of  these  tis- 
sues increases  in  the  same  order ;  but  more  important  at  present 
is  the  physiological  significance  of  these  variations  in  activity. 

Distribution  of  the  excitation  wave  in  the  auricle  is  expe- 
dited by  the  central  position  of  the  sino-auricular  node  and  by 
a  relatively  high  conduction  rate,  a  relatively  simple  plan. 
The  muscle  of  the  ventricle  conducts  slowest  because  its  func- 
tion of  distribution  is  a  minor  one;  on  the  other  hand,  this, 
the  driving  chamber,  is  provided  with  a  special  system  of  dis- 
tribution, clearly  arranged  to  provoke  almost  simultaneous  con- 
traction ;  this  special  system  is  endowed  with  conduction  powers 
of  the  highest  order. 


THE  HERTER  LECTURES 

DELIVERED  AT  THE  JOHNS  HOPKINS  HOSPITAL, 
BALTIMORE,   OCTOBER,  1914 

"  CLINICAL  MEDICINE  AND  LABORATORY 
METHODS " 

"  The  fourth  is  a  Supinity,  or  neglect  of  Enquiry,  even  of  matters  whereof 
we  doubt;  rather  believing  than  going  to  see." 

"  But  the  mortallest  enemy  unto  Knowledge,  and  that  which  hath  done 
the  greatest  execution  upon  truth,  hath  been  a  peremptory  adhesion  unto 
Authority;  and  more  especially,  the  establishing  of  our  belief  upon  the 
dictates  of  Antiquity" 

"  The  testimonies  of  Antiquity,  and  such  as  pass  oraculously  amongst 
us,  were  not,  if  we  consider  them,  always  as  exact,  as  to  examine  the  Doc- 
trine they  delivered.  For  some,  and  those  the  acutest  of  them,  have  left 
many  things  of  falsity;  controllable,  not  only  by  critical  and  collective 
Reason,  but  common  and  Countrey  observation." 

SIR  THOMAS  BROWNE. 


CHAPTER  II 

FIRST    HEtRTEK    LECTURE. 

THE  METHOD  OF  ELECTKOCABDIOGRAPHY 
EXEMPLIFIED 

Gentlemen,, 

When  your  Committee  invited  me  to  come  to  your  Anniver- 
sary meeting  and  did  me  the  honour  of  offering  me  this  lecture- 
ship, it  left  me  to  choose  the  subjects  of  my  discourses.  The 
three  lectures  which  are  to  be  given  have  been  arranged  under 
the  title  of  "  Clinical  Medicine  and  Laboratory  Methods." 
The  choice  of  this  title  seemed  to  me  the  most  fitting  for  the 
occasion,  for  it  allows  me  to  present  my  subject  matter  in  the 
form  of  a  tribute  to  your  School.  Students  of  the  Johns  Hop- 
kins University  need  no  persuasion  that  an  intimate  associa- 
tion between  the  work .  of  wards  and  laboratories  is  essential 
to-day.  You  have  been  leading  advocates  of  this  policy,  your 
institutions  are  living  monuments  to  enterprise  of  this  kind. 
You  have  indeed  the  right  to  great  pride  that  your  University 
should  have  been  the  youngest  in  the  van  of  those  promoting 
the  study  of  Medicine  upon  the  exacting  lines  of  the  scientific 
laboratory.  That  you  have  been  pioneers  is  a  matter  of  com- 
mon knowledge ;  that  you  retain  your  position  is  shown  by  your 
recent  innovation  in  Medicine,  which  all  European  schools  have 
closely  watched  with  interest  and  lively  expectancy.  If  you 
are  in  sympathy  with  the  observations  of  my  collaborators  and 
myself,  and  I  read  your  invitation  in  that  sense,  you  are  so,  if 
I  may  presume  to  say  so,  because  our  work  has  been  along  lines 
which  you  have  always  approved  and  encouraged.  There  is 

35 


36  Chapter  II 

no  closer  bond  of  union  between  fellow-workers  than  the  knowl- 
edge that  the  methods  which  they  pursue  are  harmonious,  that 
the  trains  of  thought  are  of  a  kind.  Laboratory  methods  as 
applied  to  the  study  of  clinical  medicine  have  come  to  stay; 
instruments  and  methods  of  precision  are  gradually  relieving 
medicine  of  its  past  stigma ;  they  are  lifting  it  to  the  plane  of 
its  sister  sciences,  its  true  and  proper  status.  We  have  been 
too  content  in  the  past  with  opinion,  in  the  future  we  shall  rest 
our  case  upon  fact ;  our  philosophy  takes  shape  as  it  is  moulded 
with  additional  and  certain  knowledge.  To  my  colleagues  in 
this  field,  I  would  say,  our  fight  is  not  yet  done,  there  lies 
before  this  generation  a  grand  opportunity,  a  successful  struggle 
for  freedom.  Let  us  go  forward  in  a  progressive  spirit,  cast- 
ing from  us  the  fatal  traditions  which  dog  our  footsteps.  The 
history  of  medicine  is  a  history  darkened  by  the  dust  of  faith 
and  superstition.  Our  abode  is  still  unclean;  the  broom  has 
yet  to  sweep  the  house  again ;  let  us  retain  it  in  our  hands  till 
its  appointed  task  is  done;  there  are  many  dusty  corners,  the 
cobwebs  still  cling  thickly  to  the  rafters. 

Yours  is  a  new  country;  young  workers  in  older  countries 
look  to  you  to  lead  where  they  may  follow;  they  see  you  lead- 
ing where  some  day  they  aspire  to  follow.  They  send  you  this 
message,  to  continue  to  be  their  guide  in  the  final  emancipation 
of  Medicine  as  Science. 

I  would  awaken  profound  distrust  of  authoritative  utter- 
ances, especial  distrust  of  suggestive  but  unproved  doctrines; 
our  traditional  teachings  teem  with  them;  let  each  statement 
receive  support  to  the  hilt,  evidence  is  never  too  complete. 

It  has  been  my  lot  recently  to  examine  some  old  established 
faiths  in  respect  of  cardiac  hypertrophies.  I  do  not  propose 
to  speak  of  them  at  the  present  time.  The  method  has  been 
similar  to  Miiller's,  accurate  weighing  of  the  separate  heart 
chambers.  What  the  result  ?  Little  beyond  sweeping ;  the 
destruction  of  one's  belief  in  the  power  to  gauge  preponderance 


The  Method  of  Electrocardiograph?/  Exemplified     37 

of  this  or  that  heart  chamber  by  bedside  tests;  the  conviction 
that  mechanical  factors  are  not  the  sole,  nay,  oftentimes  not  the 
chief  agents  at  work;  a  clear  appreciation  that  the  whole  sub- 
ject must  be  reopened  to  new  and  more  exacting  investigation. 
It  has  also  been  my  lot  to  join  in  investigating  certain  forms  of 
breathlessness,  and  to  this  subject  I  propose  to  devote  a  later 
lecture.  If  you  agree  with  the  conclusions  which  I  shall  then 
draw,  you  will  again  see  that  it  is  urgently  necessary  for  us  to 
revise  our  ideas  in  respect  of  dyspnoea.  So  in  many  other 
directions  our  information  is  scanty  or  ill-founded;  it  is  so  be- 
cause we  have  been  content  to  listen  to  the  voices  of  old  times, 
because  we  have  failed  clearly  to  appreciate  that  workers  of 
the  past  were  fearfully  crippled  by  lack  of  means  to  solve  the 
problems  with  which  they  wrestled;  because  in  our  hearts  we 
have  refused  to  believe  in  Medicine  as  an  exact  science. 

There  is  a  field  of  clinical  medicine  in  which  progress 
has  of  recent  years  been  considerable;  so  considerable  that 
perhaps  we  are  unable  fully  to  grasp  its  significance  at  the 
present  time.  It  is  that  which  has  refined  our  knowledge 
of  movements  of  the  heart  chambers.  If  you  took  a  clock  to 
a  mechanic  for  repairs  and  forbad  him  to  remove  its  case,  you 
could  readily  conceive  his  predicament ;  a  similar  problem  is 
presented  to  each  of  us  when  confronted  by  a  patient  with  heart 
disease.  The  mechanism  of  the  heart,  like  the  mechanism  of 
the  clock,  has  been  veiled  from  view;  listening  to  its  sounds, 
we  might  gauge  its  pulse,  as  a  child  listens  with  wonder  and 
bewilderment  to  the  ticking  of  a  watch,  or  eagerly  scans  the 
circulation  of  its  hands. 

Labouring  under  these  conditions,  an  instrument  of  pre- 
cision has  been  placed  at  our  command,  an  instrument  which 
permits  us  to  record  the  inner  workings  and  brings  us  into 
direct  contact  with  its  wheels.  This  instrument  is  the  string 
galvanometer  of  Einthoven. 

It  is  not  possible  in  this  lecture  to  cover  the  subject  of  electro- 


38  Chapter  11 

cardiography ;  it  is  possible  only  to  choose  some  few  of  the 
outstanding  problems  which  have  been  elucidated  largely  by 
its  aid.  Those  chosen  have  been  chosen  chiefly  to  illustrate 
method,  and  especially  to  confirm  your  conviction  that  clinical 
disorders  may  be  imitated  and  studied  in  the  laboratory.  It  is 
a  common  misconception  that  the  study  of  irregularities  of 
the  heart's  action  ends  with  irregularity ;  that  is  far  from  being 
the  case.  It  may  be  unhesitatingly  stated  that  graphic  methods 
are  slowly  but  surely .  altering  our  whole  conception  of  cardiac 
disease;  the  chapters  which  deal  with  cardiac  syncope,  palpita^ 
tion,  acute  dilatation,  heart  strain,  the  diagnosis  of  myocardial 
disease,  and  cardiac  failure  are  to  be  rewritten  in  the  light  of 
modern  observations.  But  we  owe  them  other  and  greater 
debts.  Graphic  work  has  dealt  as  severe  a  blow  to  the  prestige 
of  anatomical  pathology  as  any  it  has  received  of  late  years. 
Xot  that  I  desire  to  deprecate  this  line  of  study;  but  clearly, 
as  our  prime  business  is  with  the  living  and  not  with  the  de- 
funct organism,  so  the  pathology  of  the  wards  must  take  pre- 
cedence to  that  of  the  dead  house.  Graphic  records  are  records 
of  function,  normal  or  pervert ;  it  is  of  pervert  function 
that  our  patients  complain.  Graphic  work  sharpens  our  per- 
ceptions, it  provides  facts  which  are  intensely  satisfactory  as  a 
basis  for  argument.  The  records  are  clear  messages  writ  by 
the  hand  of  disease,  permanent  and  authentic  documents  which 
silence  dogma. 

The  physiological  electrocardiogram  is  as  you  know  a  direct 
record  from  the  muscle  of  the  heart,  a  record  of  the  electrical 
changes  associated  with  its  beating.  Inquire  of  this  instru- 
ment the  nature  of  the  heart  beat  in  a  normal  subject,  it  in- 
scribes a  hieroglyphic  of  the  form  which  I  now  show  you  (Fig. 
24).  Our  first  task  is  to  learn  the  meaning  of  this  strange 
writing;  our  Rosetti  stone  is  the  heart  of  the  lower  animals. 
If  we  record  the  movements  of  the  separate  chambers  of  the 


The  Method  of  Electrocardiograph^  Exemplified     39 


Fig.  24.  Simultaneous  venous,  arterial  and  electrocardiograph} c  curves, 
taken  from  a  normal  human  subject.  Illustrating  the  method  of  re- 
cording the  movements  of  the  several  heart  chambers.  "  a "  in  the 
venous  curve,  P  in  the  electrocardiogram,  represent  the  activity  of  the 
auricle.  "  c  "  and  "  v  "  in  the  venous  curve,  Q,  R,  S  and  T  in  the  elec- 
tric curve,  represent  systole  of  the  ventricle. 


Pig.  25.  An  electrocardiogram  from  a  dog  with  simultaneous  curves  from 
auricular  and  ventricular  muscle;  to  show  how  the  relations  of  elec- 
trocardiographic  deflections  to  muscular  events  are  studied. 


40  Chapter  II 

dog's  heart,  and  allow  our  galvanometer  simultaneously  to  write 
its  message  (Fig.  25),  we  find  it  speaks  of  two  events;  it  re- 
cords the  activity  of  the  auricles  and  of  the  ventricles.  The 
deflection  P  is  the  representative  of  auricular  activity,  though 
it  slightly  precedes  the  contraction ;  the  deflections  R,  S,  and 
T  speak  for  the  activity  of  the  ventricles.  The  instrument  not 
only  signals  these  chief  events,  it  tells  us  if  the  sequence  of 
contraction  in  the  muscle  elements  of  a  given  chamber  is  nor- 
mal. The  normal  curve  P  is  given  by  a  contraction  coursing 
along  normal  auricular  paths  only;  the  usual  deflections  R,  8 
and  T  by  a  beat  following  physiological  paths  in  the  ventricle 
only.  Abnormal  beats  of  either  chamber  are  portrayed  by 
curves  of  peculiar  and  distinctive  forms.  In  a  given  case  the 
type  of  curve  is  controlled  by  the  direction  of  contraction  in  the 
muscle,  relative  to  the  position  of  the  contacts  upon  the  body ; 
it  is  controlled  therefore  by  the  point  at  which  the  contraction 
originates.  Let  me  illustrate  these  statements,  which  are  the 
first  grammatic  rules  of  this  new  language. 

In  the  first  example  which  I  show  you  are  two  curves;  the 
one  (Fig.  26)  taken  from  a  patient  who  exhibited  a  regular 
coupling  of  the  pulse  beats.  The  electrocardiographic  curves 
show  the  same  coupling,  and  each  beat  of  a  couple  consists  of 
an  auricular  portion  P  and  of  a  ventricular  portion,  R,  8  and 
T.  It  is  an  example  of  an  irregularity  due  to  what  are  known 
as  auricular  extrasystoles.  But  if  you  examine  the  curve  in  de- 
tail, you  see  that  the  second  beat  of  each  couple,  the  premature 
one,  resembles  the  first  beat  of  each  couple  in  every  respect ;  first 
and  second  beats  have  followed  the  same  muscle  paths  and  the 
disturbance  which  gives  rise  to  the  second  beat  must  have  had  its 
seat,  if  our  rule  holds  true,,  in  that  portion  of  the  heart  from 
which  the  first  or  normal  beat  arose.  That  this  is  so  is  shown 
by  the  next  curve  (Fig.  27).  It  is  an  experimental  replica 
of  the  first,  and  was  produced  by  stimulating  the  heart  at  the 
seat  of  natural  impulse  formation.  A  duplicate  could  be  pro- 


The  Method  of  Electrocardiograph^  Exemplified     41 

duced  in  no  other  fashion.  This  is  our  method,  to  attempt  to 
produce  disturbances  in  the  experimental  heart,  parallel  to  those 
which  we  see  in  the  clinical  heart.  Our  first  clinical  example 
is  one  in  which  we  may  locate  a  process  of  irritation  in  a  given 
region  of  the  right  auricle,  namely,  in  the  immediate  neighbour- 
hood of  the  sino-auricular  node,  the  structure  which  forms  the 
natural  pacemaker  of  the  heart.  My  second  illustration 


s 


P*T 


p  f 

1S  5 


Fig.  26  and  27.  Two  curves  showing  coupled  action  of  the  heart  beat,  the 
first  from  a  patient,  the  second  from  a  dog.  The  coupled  action  in  the 
experimental  instance  resulted  from  stimulation  of  the  auricle  in  the 
region  of  the  superior  cava.  To  illustrate  the  method  of  investigat- 
ing the  origin  of  irregular  heart  action  in  clinical  subjects. 

similar  (Fig.  28).  Here  is  an  electrocardiogram  from  a  pa- 
tient who  exhibited  an  intermittence  of  the  pulse  and  whose 
electrocardiograms  not  only  portrayed  numerous  beats  of  nor- 
mal outline  but  the  curious  atypical  beats  which  give  such  large 
excursions.  For  comparison  with  this  curve  is  one  of  experi- 
mental origin  (Fig.  29)  and  the  resemblance  between  the  two 
is  close.  The  experimental  curve  is  written  side  by  side  with 
curves  of  mechanical  shortening  in  auricle  and  ventricle,  a 
script  with  which  we  are  long  familiar.  The  experimental 
irregularity  was  produced  by  stimulating  the  right  ventricle. 


42 


Chapter  II 


The  disturbance  is  confined  to  the  ventricle  as  the  mechanical, 
records  demonstrate,  for  the  auricular  rhythm  throughout  is 
undisturbed.  The  atypical  beats  which  have  arisen  prema- 
turely in  the  right  ventricle,  in  virtue  of  their  abnormal  origin, 


m   m  *     T      r 


Fig.  28.     A  clinical  curve  showing  an  irregularity  of  the  heart's  action. 

As, 


Fig.  29.  A  similar  experimental  electrocardiogram  accompanied  by  curves 
of  shortening  of  the  auricular  and  ventricular  muscle;  the  atypical 
beats  were  produced  by  stimulating  the  right  ventricle. 

have  pursued  an  abnormal  course  through  the  muscle  of  the  ven- 
tricle; it.  is  to  this  that  the  changed  character  of  the  corre- 
sponding curves  is  due.  It  is  in  the  manner  illustrated  that 
the  seat  of  disordered  heart  action  has  been  analysed. 


The  Method  of  Electrocardiograph^  Exemplified     43 

I  show  you  another  clinical  example  of  a  curious  change  in 
the  action  of  the  heart.  The  first  few  beats  of  Fig.  30  are  of 
normal  type,  the  auricle  and  ventricle  are  beating  in  their 
usual  sequence;  but  as  the  rhythm  proceeds,  its  rate  slows  a 
little  and  suddenly  the  auricular  summits  disappear.  We 


Fig.  30.     A  clinical  curve  showing  escape  of  the  A-V  node  as  a  result  of 
slowing  of  the  natural  rhythm. 


•;\J  |      -\\Jki  ^PiilN         M-^  :         I    >"W:         i      >— | 


/t*  •   jrf  •      fj  t    joj  I  &  *  t  rt      { 

rj    1  fy  .  .  ~~  I        t.   *   *\!  ;  17  j  nt       '','t^'^1'11-          1 1*\      I 

T  \   rrnl      T  71 


Fig.  31.  An  experimental  curve  showing  similar  slowing  of  the  heart  and 
escape  of  the  A-V  node  when  the  sino-auricular  node  is  depressed  by 
cooling. 

should  possess  no  clue  to  the  nature  of  this  change  had  we  no 
experimental  data  for  comparison.  The  meaning  of  it  is 
clearer  when  we  study  the  companion  curve  (Fig.  31).  Here 
we  have  electrocardiogram  and  mechanical  curves,  written 
simultaneously  from  the  exposed  heart  of  a  dog.  formally  the 


44  Chapter  II 

heart  beat  starts  in  the  region  of  the  mouth  of  the  superior  cava 
in  a  structure  termed  the  sino-auricular  node  (see  Chapter 
I).  If  you  depress  the  physiological  activity  of  this  struc- 
ture by  cooling,  you  obtain,  as  Ganter  and  Zahn  have  shown,  a 
retardation  of  heart  rate,  and  before  long  the  auricular  sum- 
mits P  are  lost.  They  are  lost,  as  the  experimental  curve 
shows  clearly,  because  the  contractions  of  auricle  and  ventricle 
are  no  longer  in  sequence  but  simultaneous,  the  auricular  curve 
being  buried  and  hidden  in  the  ventricular  curve.  As  the 
activity  of  the  normal  pacemaker  becomes  depressed  by  cooling, 
other  centres  become  relatively  more  active,  and  the  first  in  the 
race  for  control  of  the  heart  beat  is  the  auriculo-ventricular 
node,  which  lies  in  the  path  between  auricle  and  ventricle. 
When  the  upper  node  is  cooled,  the  central  node  becomes  the 
most  active  and  dominates  the  heart's  movements.  Each  time 
it  produces  a  rhythmic  impulse,  this  impulse  travels  to  auricle 
and  to  ventricle  simultaneously,  the  systoles  of  auricle  and  ven- 
tricle synchronise  and  yield  this  abnormal  electrocardiogram. 

I  have  spoken  of  the  A-V  node ;  it  is  the  first  part  of  a  system 
of  fibres  which  joins  the  auricles  to  the  ventricles,  the  system 
as  a  whole  serving  as  a  channel  of  conduction  for  impulses 
passing  from  one  chamber  to  the  other.  It  is  largely  to  work 
carried  out  in  your  institute  by  Erlanger  and  his  collaborators 
that  we  owe  our  knowledge  of  the  functions  of  this  delicate 
strand  of  tissue,  called  the  A-V  bundle  or  bundle  of  His.  The 
ventricle  depends  for  its  impulse  to  contract  upon  the  auricle 
and  upon  the  integrity  of  this  tract.  If  the  bundle  is  damaged 
by  injury  or  disease,  co-ordination  between  the  two  chief  di- 
visions of  the  heart  is  disturbed.  I  show  you  a  series  of  curves 
which  illustrate  this  disorder;  a  clinical  curve  (Fig.  32),  and 
two  experimental  examples.  Heart-block  as  it  is  termed  may 
be  produced  in  a  variety  of  ways.  It  has  been  shown  to  follow 
when  the  bundle  is  pressed  upon  or  crushed,  by  Erlanger  and 
Hirschfelder,  your  experimentalists.  It  comes  when  the  track 


The  Method  of  Electrocardiograph^  Exemplified     45 

is  damaged  in  any  way,   be  this  damage  deliberate  or  be  it 
through  the  accident  of  disease.     It  may  be  caused  by  the  in- 


Fig.  32.     A  clinical  instance  of  heart-block  in.  a  patient  who  suffered  from 
chronic  myocardial  disease. 


Fig.  33.     The  heart  beat  of  a  cat  recovering  from  asphyxia.     A  period  of 
2  :  1  heart-block  passes  into  the  natural  rhythm. 


T  f*     7~  p     T  f>        P     -r  f>      ~r 


Fig.  34.     Venous,    arterial    and    electrocardiographic    curves    from    a    dog, 
showing  heart-block  as  a  result  of  stimulating  the  left  vagus. 

troduction  of  poisons  into  the  circulation,  such  for  example  as 
diphtheria  toxine,  digitalis  or  the  products  of  asphyxia  (Fig. 
33).  It  is  produced  by  stimulation  of  the  vagus,  more  espe- 


46  Chapter  II 

cially  the  left  nerve  (Fig.  34).  All  these  methods  of  produc- 
ing block  experimentally  have  clinical  parallels.  The  most 
important  are  those  in  which  definite  lesions  are  to  be  found 
in  the  bundle  region.  The  bulk  of  the  ventricular  muscle  is 
silent  in  disease;  affections  of  the  bundle  or  its  branches  tell 
us  often  of  an  active  or  chronic  process  in  the  myocardium. 
As  you  know,  heart-block  is  responsible  for  one  of  the  major 
forms  of  cardiac  syncope;  where  a  slow  pulse  action  is  accom- 
panied by  attacks  of  loss  of  consciousness  (Adams-Stokes  Syn- 
drome). It  is  experiment,  and  experiment  only,  which  has 
taught  us  the  clinical  varieties  of  this  condition. 

We  come  to  the  most  frequent  and  important  disorder  of  the 
human  heart  beat,  that  so  familiar  to  you  as  an  accompaniment 
of  failure  of  the  muscle.  The  irregularity  of  the  pulse  which, 
on  account  of  its  complexity,  has  given  rise  to  the  term  delirium 
cordis,  was  one  of  the  last  to  receive  adequate  explanation;  it 
has  been  studied  since  the  active  days  of  Marey,  Sommerbrodt 
and  Riegel.  The  first  clue  to  its  real  meaning  came  from  two 
laboratory  workers  in  this  land,  Cushny  and  Edmunds;  it  is 
now  definitely  known  to  result  from  what  is  termed  fibrillation 
of  the  auricles.  That  knowledge  has  been  gained  directly  and 
exclusively  from  animal  experiment,  conducted  side  by  side 
with  clinical  observations.  Without  such  experiment  we  could 
have  gathered  no  true  conception  of  the  events  in  the  heart. 
This  discovery  has  explained  a  multitude  of  obscure  phenomena, 
it  will  continue,  if  I  mistake  not,  to  shed  light  upon  the  path- 
ology of  heart  disease  for  many  years  to  come.  When  the 
auricles  pass  into  fibrillation  they  cease  to  beat  and  their  walls, 
standing  in  a  position  of  diastole,  exhibit  small  flickering 
tremulous  movements,  which  are  the  expression  of  inco-ordinate 
activity.  Their  function  of  propelling  blood  to  the  ventricles 
is  lost ;  they  no  longer  serve  as  reservoirs  while  the  ventricle  is 
contracted;  the  blood  stagnates  perpetually  in  them,  the  forma- 
tion of  muscle  clots  is  promoted ;  heart  murmurs  become 


The  Method  of  Elect  rocardiograpliy  Exemplified     47 

altered;  such  activity  as  the  auricle  possesses  is  expressed  in 
a  malignant  fashion,  it  lashes  the  ventricle  to  a  quick  and  dis- 
ordered movement,  exposing  any  weakness  of  the  ventricular 
muscle,  if  such  exists,  for  the  muscle  cries  out  against  the  in- 
creased strain.  The  arterial  blood  pressure  sinks,  venous  pres- 
sure rises ;  the  onset  of  this  condition  is  the  most  important 
contributory  cause  of  cardiac  failure  of  which  we  have  real 


Fig.   35.     A  clinical  curve  from  a  case  of  mitral  stenosis  and  muscle  fail- 
ure, illustrating  fibrillation  of  the  auricles. 


Fig.  36.     Venous,  arterial  and  electrocardiographic  curves  from   a   dog  in 
which  the  auricles  had  been  forced  to  fibrillate  by  faradisation. 

knowledge.  It  was  the  electrocardiograph  which  first  bore 
clear  witness  of  its  occurrence  in  the  human  subject.  I  show 
you  two  curves,  clinical  and  experimental  exainples  for  com- 
parison (Figs.  35  and  36).  You  will  notice  the  irregularity 
of  the  ventricle  in  each,  the  absence  of  true  auricular  summits 
P,  their  replacement  by  the  oscillations  which  characterise  the 
condition.  These  oscillations  are  proved  to  arise  in  the  auricle ; 


48  Chapter  II 

they  represent  the  sum  total  of  its  delirious  activity.  The 
curves  of  fibrillation  are  of  varied  form,  both  in  experiment  and 
in  human  disease.  Further  examples  are  shown  in  Figs.  37 
and  38.  In  Fig.  36  the  auricular  delirium  was  produced  by 
faradisation  of  the  auricles;  Fig.  37  is  a  clinical  curve;  that 
of  Fig.  38  resulted  from  the  introduction  of  a  poison  into  the 


Fig.  37.     Spontaneous  fibrillation  in  the  human  subject  in  "ft  case  erf  "rheu- 
matic heart  disease. 


-2T 


Fig.  38.     Fibrillation  of  the  auricles  produced  experimentally  by  the  in- 
jection of  glyoxyllic  acid. 

blood  stream  of  an  animal.  We  are  still  far  from  a  full  knowl- 
edge of  the  pathology  in  the  human  subject,  but  the  first  and 
important  steps  of  isolating  and  recognising  its  true  meaning 
have  been  taken  finally.  What  its  isolation  means  to  us  may 
be  grasped  when  its  prognostic  significance  is  appreciated,  and 
when  its  almost  specific  reaction  to  drugs  of  the  digitalis  group 
is  realised.  It  is  from  the  reaction  of  the  heart,  affected  in 
this  fashion,  that  digitalis  owes  its  wide  reputation;  it  is  in 
these  cases  that  it  grips  the  heart  and  gives  the  slowing  of 
pulse  rate  which  relieves  an  exhausted  muscle. 

You  will  find  clear  instances  of  this  affection  described  in 
Da  Costa's  historic  treatise  upon  the  irritable  heart  of  soldiers ; 
it  has  since  passed  on  numerous  occasions  as  an  instance  of  heart 


The  Method  of  Electrocardiograph^  Exemplified     49 

strain.  You  will  see  patients  in  whom,  occurring  as  a  tem- 
porary disorder,  it  promotes  acute  dilatation  of  the  heart,  and 
YOU  will  hear  the  term  "  dilatation  "  applied  as  the  diagnosis  in 
the  case.  It  is  but  recently  that  we  have  appreciated  that  the 
fibrillation  is  the  cause  of  the  disturbance,  and  that  the  irregu- 
larity is  not  the  sequel  of  distention  of  the  heart.  You  will 
meet  cases  in  which  as  a  fleeting  and  recurring  disorder  it 


Fig.  39.     Auricular  nutter  occurring  in  a  clinical  case. 


Fig.  40.     The  end  of  a  period  of  flutter,  produced  in  a  dog  by  the  injec- 
tion of  glyoxyllic  acid  into  the  blood  stream. 

promotes  constant  palpitation  or  even  temporary  loss  of  con- 
sciousness. You  will  meet  it  daily  in  your  work  as  an  asso- 
ciate and  chief  promoter  of  chronic  heart  failure.  You  will 
recognise  it  clinically  because  of  this  frequent  association,  be- 
cause it  is  the  only  common  irregularity  which  consorts  with 
rapid  heart  action,  because  the  ventricular  beating  is  tumultu- 
ous and  never  constant  from  moment  to  moment.  The  ability 
to  recognise  it  is  a  prime  asset  to-day  in  dealing  with  grave 
cardiac  affections. 

Our  most  recent  acquisition  is  "  auricular  flutter  "  (Figs. 
39  and  40).  In  elderly  subjects  a  persistent  and  considerable 
acceleration  of  the  heart's  action  may  be  found,  but  unlike  the 
acceleration  of  fibrillation,  this  acceleration  is  associated  as  a 
general  rule  with  regular  action.  In  many  of  these  patients, 


50 


Chapter  II 


galvanometric  curves  lay  bare  an  unsuspected  and  astonishing 
fact.  While  the  ventricle  beats  regularly  at  from  130  to  170, 
the  auricular  rate  is  precisely  double.  That  the  auricles  may 
beat  at  rates  of  300  or  350  per  minute,  and  that  such  hyper- 
activity  may  be  maintained  for  years,  would  have  received  no 
credence  a  few  years  since;  it  is  now  established.  A  clin- 
ical example  of  flutter,  as  it  is  termed,  is  to  be  seen  in  Fig. 


Fig.  41.  Venous,  arterial  and  electroeardiographic  curves  from  a  case  of 
auricular  flutter.  The  pulse  beats  regularly  at  60,  the  jugular  curve 
shows  little  or  no  sign  of  the  auricular  contractions.  The  electrocar- 
diogram demonstrates  a  regular  auricular  rate  of  240  per  minute. 

39,  where  the  respective  rates  of  auricle  and  ventricle  are  228 
and  114.  The  ventricle  beats  in  response  to  each  second  auric- 
ular contraction ;  nutter  'generally  exhibits  this  associated  heart- 
block,  the  ventricles  fail  to  respond  to  the  highest  auricular 
rate.  It  may  be  associated  with  higher  grades  of  block, 
whereby  the  ventricular  rate  is  reduced  perhaps  to  normal  limits 
and  further  concealed.  The  value  of  our  laboratory  method 
cannot  be  more  clearly  illustrated  than  by  clinical  cases  of  this 
type.  On  several  occasions  I  have  examined  patients  when  the 
ventricle  and  pulse  were  beating  regularly  at  perfectly  normal 
rates,  and  in  whom  no  suspicions  of  the  auricular  rate  were  awak- 


The  Method  of  Electrocardiograph^/  Exemplified     51 

ened  until  the  heart  was  submitted  to  this  electrocardiographic 
test.  Fig.  41  is  from  a  case  of  this  kind;  it  discloses  an  un- 
suspected auricular  rate  of  240  per  minute;  the  pulse  rate  is 
60  per  minute.  Kow  these  cases  of  auricular  nutter,  where 
there  is  extreme  though  regular  acceleration  of  auricle,  are  not 
so  infrequent  as  we  at  first  supposed;  the  affection  is  a  serious 
one,  for  even  though  the  ventricular  rate  is  but  half  the  auric- 
ular, it  is  usually  very  fast  and  taxes  an  unhealthy  or  aged  heart 
to  the  utmost ;  moreover,  there  is  a  constant  risk  in  many  such 
cases  that  the  ventricle  may  respond  to  the  faster  rate  and  that 
an  intolerable  burden  may  thus  be  imposed  upon  it.  It  is  a 
fortunate  thing  that  we  have  a  sure  remedy  for  such  patients; 
flutter  has  affinities  with  fibrillation,  for  digitalis  will  slow  the 
ventricle  and  maintain  its  rate  within  bounds  in  flutter  as  in 
fibrillation ;  the  drugs  acts  by  increasing  the  pre-existing  heart- 
block.  I  have  seen  no  patient  in  whom  this  reaction  could  not 
be  obtained,  and  in  many,  so  I  find,  the  reaction  may  be  carried 
a  step  farther.  If  digitalis  is  pushed  and  is  tolerated,  the 
auricles  pass  from  flutter  to  the  higher  grade  of  disorder, 
fibrillation.  You  might  think  the  effect  undesirable,  in  re- 
ality that  is  not  the  case.  Flutter  is  essentially  a  persist- 
ent condition  and  untreated  may  be  maintained  during  the 
rest  of  the  patient's  life.  Change  the  mechanism  by  the  ex- 
hibition of  digitalis  and  the  production  of  fibrillation,  and, 
having  accomplished  this  end,  relax  the  drug ;  the  heart  returns, 
not  to  flutter,  but  to  the  normal  rhythm.  I  well  remember  the 
first  case  in  which  this  reaction  was  clearly  demonstrated.  It 
was  in  a  French  polisher  admitted  to  hospital  with  a  ventricular 
rate  of  160 ;  the  auricles  were  beating  at  320  per  minute  (Fig. 
42a).  Upon  digitalis  the  pulse  fell  rapidly  to  80,  the  auricular 
rate  persisting  as  before  (Fig.  42&).  An  increase  of  the  dose 
now  caused  the  onset  of  fibrillation  (Fig.  42c),  when  the  drug 
was  withdrawn  the  normal  rhythm  was  restored  within  a  short 
time  (Fig.  42d).  The  man  was  admitted  with  all  the  classical 


52 


Chapter  II 


P  '  P    P    P 


- 


rrnr'tt*^ 


tHiiHiHHilliilittt^ 


itiiiniini.tiiuiiitn?iniiiitttttniinritinnirtitttninitiitMititiutMti-rTnninmrtnrTnn.tnHHtrnnt 


Fig.  42.  a,  6,  c  and  c?.  Four  curves  from  a  patient  who  exhibited  auricu- 
lar nutter,  (a)  Before  treatment;  the  auricular  rate  is  320,  the 
ventricular  160  per  minute.  (&)  While  upon  digitalis;  the  auricular 
rate  is  still  320;  the  ventricle  beats  at  80  per  minute,  (c)  After 
pushing  digitalis,  the  auricles  fibrillate;  eventually,  after  relaxing  the 
drug  the  normal  rhythm  is  restored  (d) . 

signs  of  cardiac  failure,  he  returned  to  work.  Some  few 
months  later  the  flutter  returned,  but  being  treated  once  more 
in  the  same  fashion,  it  was  again  abolished.  That  is  three 
years  since  and  our  patient  is  still  in  comfortable  health  and 
fully  engaged  in  his  trade. 


CHAPTER  III 

SECOND    HERTER   LECTURE 

THE  KELATIOJST  OF  AURICULAR  SYSTOLE  TO 
HEART  SOUNDS  AND  MURMURS 

Gentlemen, 

The  subject  with  which  I  propose  to  deal  to-day  as  my  second 
illustration  of  the  application  of  laboratory  method  to  the  clin- 
ical case  is  that  of  the  graphic  registration  of  heart  sounds. 
And  this  subject  has  been  selected  from  two  points  of  view. 
Eirst  of  all,  because  phonograms  provide  us  with  pictorial 
representations  of  auscultatory  signs  and  have  no  inconsid- 
erable value  in  this  respect  for  teaching  purposes.  A  few 
selected  phonograms  accompanied  by  accurate  descriptions 
bring  home  to  the  student  the  nature  of  the  signs  which  he  ob- 
serves, and  impress  the  simpler  lessons  of  acoustics  in  a  facile 
and  clear  cut  fashion.  The  sounds  conveyed  from  chest  by 
stethoscope  to  ear  set  in  motion  the  tympanic  membrane;  they 
cause  the  recording  instrument  to  vibrate  in  a  similar  fashion. 
There  is  however  an  important  distinction  between  the  impres- 
sion gained  from  the  writing  on  paper  as  we  see  it  and  those 
which  come  to  us  through  the  more  direct  channels  of  the 
auditory  nerves.  To  those  who  are  accustomed  to  inscribe  these 
records  and  also  to  listen  to  the  beating  heart,  having  experi- 
ence of  its  sounds,  nothing  is  more  impressive  than  the  ability 
of  the  brain  to  discriminate;  attention  is  concentrated  for  the 
moment  upon  sounds  of  one  kind,  perception  of  interfering 
sounds  is  meanwhile  largely  or  wholly  in  abeyance.  A  delicate 
phonograph  records  all  sound  vibrations  transmitted  to  it,  be 
they  of  cardiac,  respiratory  or  extrinsic  origin;  a  short  and 

53 


54  Chapter  HI 

combined  experience  of  recorder  and  stethoscope  soon  gives 
prominence  to  a  fact  which  to  a  student,  as  he  becomes  clinician, 
rapidly  recedes  to  the  background ;  the  living  chest  is  filled  with 
a  babel  of  tongues,  the  sympathetic  ear  heeds  one  voice.  So  it 
happens,  when  we  scan  our  first  acoustic  records,  that  their  com- 
plexity bewilders  us,  and  to  analyse  them  we  confine  ourselves 
at  first  to  the  more  simple  documents,  and  especially  to  those 
which  represent  in  a  relatively  pure  form  the  sounds  which  we 
propose  to  study.  But  the  lesson  is  not  lost;  our  admiration 
for  the  delicacy  of  the  auditory  mechanism  is  a  thousandfold 
enhanced,  and  we  learn  that  in  the  discrimination  of  pitch, 
tone  and  intensity,  the  physiological  ear  has  no  rival.  These 
remarks  bring  me  to  the  statement  of  my  second  object.  It  is 
to  show  that  although  the  ear  has  this  unquestioned  superiority, 
and  that  although  the  auscultatory  signs  of  heart  disease  have 
been  minutely  studied  by  its  means  and  by  countless  workers, 
we  have  yet  much  to  learn  and  much  which  can  be  learned  only 
by  the  employment  of  mechanical  aids.  The  chief  value  of  the 
recorded  heart  sound  is  the  possibility  of  accurately  timing  its 
occurrence  in  relation  to  the  events  of  the  cardiac  cycle. 

It  is  not  my  purpose  to  consider  the  history  of  sound  records, 
neither  shall  I  attempt  to  cover  a  hundredth  part  of  the  whole 
field  of  fact  and  speculation  surrounding  heart  sounds  and  mur- 
murs ;  but  I  shall  be  content  to  describe  in  simple  terms  a  single 
device,  and  to  pass  to  brief  descriptions  of  some  recent  observa- 
tions which  seem  to  show  how  important  the  influence  of  the 
auricular  pressure  upon  sounds  and  murmurs  may  be. 

In  the  first  figure  (Fig.  43)  a  tuning  fork  is  represented  as 
emitting  sound;  with  each  movement  of  the  fork  towards  the 
right,  the  air  in  this  direction  becomes  compressed;  the  tension 
is  relieved  in  every  direction,  amongst  others  towards  the  re- 
cording instrument ;  it  travels  through  the  atmosphere,  fading 
as  it  travels,  as  does  a  ripple  on  the  surface  of  water;  as  the 
fork  returns  from  its  swing,  the  same  neighbouring  air  becomes 


55 


Relation  of  Auricular  Systole  to  Heart  Sounds 

rarefied  and  this  rarefaction  follows  the  wake  of  the  condensa- 
tion and  is  transmitted  through  space.  At  a  given  moment, 
therefore,  the  air  surrounding  the  fork  is  arranged  in  alternate 
layers  of  condensation  (Co)  and  rarefaction  (Ra)  ;  each  and  all 


Fig.  43.  A  diagram  of  a  vibrating  tuning  fork,  the  sound  oscillations 
from  which  are  recorded  by  a  microphone  (M).  The  microphone  con- 
sists of  carbon  plate  (PI. )  and  point  (Pi.)  and  these  are  in  circuit 
with  a  battery  (B)  and  the  primary  coil  of  an  inductoriinn.  The  sec- 
ondary coil  is  directly  connected  to  the  string  galvanometer. 

are  travelling  along  radiating  lines.  Our  recorder  contains  a 
thin  carbon  plate  (PI),  which  being  sensitive  to  movement, 
oscillates  ,in  synchronism  with  the  condensations  and  rarefac- 
tions as  they  arrive;  it  is  the  oscillation  of  this  plate  which 
yields  the  record,  as  it  is  the  similar  oscillations  of  the  tympanic 
membrane  which  convey  the  auditory  impression  of  sound; 
for  the  alternate  layers  in  the  air  form  the  sound  vibrations. 
The  movements  of  the  plate  are  traced  by  allowing  it  to  rest 
against,  a  carbon  point  (Pi)  and  by  recording  the  changes  in 
resistance  which  occur  between  the  two  carbon  surfaces  as  the 
pressures  between  them  vary.  For  this  purpose  a  constant  cur- 
rent is  transmitted  from  carbon  to  carbon  and  in  the  same  cir- 


56  Chapter  111 

cuit  a  primary  coil  is  placed.  The  resistance  between  carbon 
and  carbon  varies  as  succeeding  phases  of  the  sound  vibrations- 
reach  it,  and  so  the  current  flowing  through  the  circuit  varies; 
the  changes  in  the  current  are  magnified  by  the  secondary  coil 
and  pass  into  the  sensitive  string  galvanometer.  So  each  move- 
ment of  the  fork  is  accompanied  by  a  movement  of  the  string 
and  our  record  is  in  reality  a  record  of  the  fork's  oscillations. 
Similarly  in  taking  tracings  from  the  chest  wall,  the  sounds  are 
records  of  the  valve  vibrations  transmitted  through  the  chest 
wall  and  stethoscope  to  the  carbon  plates,  which  form  the  mi- 
crophone, and  thence  to  the  galvanometer. 

Fig.  44  is  a  record  of  the  movements  of  a  tuning  fork,  or  if 
you  will  the  sound  it  yields,  beating  regularly  at  50  per  second. 
You  see  that  the  vibrations  are  regularly  placed,  and  it  is  to 
this  regular  arrangement  that  the  sound  emitted  owes  its  musi- 
cal quality.  As  you  know,  the  pitch  is  regulated  by  the  fre- 
quence. Comparable  records  are  to  be  obtained  from  vibrating 
strings  and  from  time  to  time  the  sharp  edge  of  a  broken  valve. 
The  loud  and  musical  murmurs  which  are  not  infrequent  after 
rupture  of  the  aortic  valves  are  produced  in  this  manner;  ex- 
amples are  seen  in  Figs.  45  and  46. 

Accurate  timing  of  sounds  is  best  accomplished  by  the  sim- 
ultaneous record  of  sound  and  electrocardiogram.  The  records 
in  the  accompanying  figure  were  taken  for  the  most  part  with 
separate  galvanometers  placed  side  by  side ;  in  all  instances  the 
records  are  so  arranged  that  points  of  the  two  curves  lying  on 
the  same  vertical  line  represent  the  same  time  instant.  The 
onsets  of  first  and  second  sounds  and  their  relation  to  systole  in 
auricle  or  ventricle  may  be  estimated  by  a  comparison  of  the 
curves,  allowing  a  short  interval  in  the  electrocardiogram  for 
the  appearance  of  the  excitation  wave  before  the  contraction 
wave.  But  so  far  as  the  ventricle  is  concerned,  the  most  exact 
method  in  a  given  case  is  to  take  the  onset  of  the  recorded  first 
and  second  sounds,  where  they  are  unquestionable,  as  the 


Relation  of  Auricular  Systole  to  Heart  Sounds     57 


Fig.  44.     A  tuning  fork  record. 


Fig.  45.     Musical  to  and   fro  murmur  at  the  aortic   cartilage. 


Fig.  46.     A  diastolic  murmur  of  aortic  origin  and  musical  quality. 


Fig.  47.     Record  of  normal  apical  heart  sounds. 


58  Chapter  111 

indices  of  onset  and  offset  of  systole.  It  may  be  necessary  when 
the  record  is  complicated  by  murmurs  to  take  a  control  record 
from  the  same  case,  with  the  object  of  obtaining  the  1st  and 
2nd  sound  in  a  more  uncomplicated  form  from  a  neighbouring 
point  upon  the  chest  wall,  and  then  by  comparing  the  two 
plates,  the  necessary  data  are  obtained. 

The  relation  of  the  onset  of  the  1st  and  2nd  sounds  to  the 
electrocardiographic  deflections  is  subject  to  some  variation. 
The  1st  sound  begins  from  .002  to  .026  seconds  after  the  -com- 
mencement of  R,  or  from  .011  to  .039  seconds  after  the  com- 
mencement of  Q,  when  this  deflection  is  present.  The  2nd 
sound  may  start  .035  seconds  before,  or  as  late  as  .028  seconds 
after  the  end  of  T;  as  a  rule  it  begins  within  a  very  short  dis- 
tance of  the  end  of  T.  As  a  general  standard  we  may  use  R 
and  take  a  point  l-50th  of  a  second  after  this  upstroke ;  it  will 
represent  the  onset  of  systole  with  no  greater  error  than  1-5 Oth 
of  a  second.  Similarly,  we  may  take  the  end  of  T  as  repre- 
senting the  offset  of  systole  and  the  error  will  be  no  greater 
than  l-30th  of  a  second. 

Generally  speaking  the  natural  heart  sounds  are  complex; 
the  oscillations  are  irregular  in  time  and  amplitude,  vary- 
ing much  from  subject  to  subject.  A  relatively  simple  record 
from  a  normal  heart  is  seen  in  Fig.  47 ;  you  will  notice  that  the 
1st  sound  begins  as  a  crescendo,  rapidly  reaches  its  maximum 
and  tails  away  as  a  diminuendo.  The  2nd  sound,  as  is  usual, 
is  abrupt  in  its  onset,  consisting  as  a  whole  of  a  simple  diminu- 
endo. In  the  instance  of  the  musical  murmurs  which  I  have 
shown  you,  the  number  of  vibrations  was  138  to  180  per  second. 
The  number  for  the  natural  1st  sound  is  much  less,  being  45 
to  70  per  second,  and  for  the  2nd  sound,  40  to  86  per  second. 
This  speaks  for  the  valvular  origin  of  both  sounds  in  the  main, 
for  the  frequence  depends  upon  the  length  and  mass  of  the 
vibrating  structure  and  upon  its  state  of  tension.  Incidentally 
we  may  compare  these  sound  records  with  records  of  the  spoken 


Relation  of  Auricular  Systole  to  Heart  Sounds     59 

syllables  lub-dup  (Fig.  48)  ;  and  a  comparison  of  this  kind  at 
once  demonstrates  how  imperfect  is  this  phonetic  representa- 
tion. Both  lub  and  dup  are  in  reality  each  built  np  by  at  least 


Fig.  48.     Two  records  of  the  spoken  syllables  "  lub-dui>." 

three  distinct  vocal  acts,  though  in  rapid  speaking  there  is  some 
slurring. 

We  pass  to  our  main  topic,  the  influence  of  the  auricles  upon 
heart  sounds.  That  auricular  contractions  may  «-ive  rise  to 
audible  sounds  has  been  suspected  for  a  long  while,  that  such 
is  indeed  the  case  was  shown  after  dissociation  of  the  contrac- 
tions in  auricle  and  ventricle  was  discovered.  It  is  now  well 
known  that  in  cases  where  the  ventricle  is  beating  slowly  in 
response  to  its  own  inherent  rhythm  and  where  the  auricular 
rate  is  still  normal  and  therefore  much  faster  than  the  ven- 
tricular, the  long  diastoles  of  the  ventricle  may  not  be  silent; 
but  that  faint  thuds  may  be  heard  at  apex,  epigastrium  or  heart 
base,  which  can  only  be  attributed  to  contractions  of  the  auricles. 
This  explanation  is  clearly  justified  by  such  curves  as  that  of 
Fig.  49 ;  here  the  auricles  are  contracting  at  three  times  the 
rate  of  the  ventricles  as  the  simultaneous  electrocardiogram 
demonstrates.  In  every  diastole  the  auricles  beat  twice  and  on 
each  occasion  produce  a  faint  and  double  sound.  The  first  ele- 
ment of  this  double  sound  does  not  begin  immediately  with 


60 


Chapter  III 


auricular  systole,  but  when  the  latter  is  well  advanced;   its 

cause  is  not  clear; 
that  it  is  not  due  to 
the  passage  of 
blood  to  ventricle 
seems  evident,  for 
a  similar  sound  oc- 
"«  curs  during  the 

o  ~ 

end  of  ventricular 

§  systole     where 

a,  another    auricular 

-£  contraction     'falls. 

§  Possibly  it  is  due 

•3  to  the  actual  con- 

|  traction      of      the 

"  muscle  of  the  auri- 

£  cle  and  to  tension 

-g  in  its  walls.     The 

§  second   element   is 

C/3 

~       I    think    attribut- 

ct 

1      able  to  the  cessa- 
s       tion  of  flow  from 
^       auricle  to  ventricle 
^       and  to  consequent 
5;       closure  of  the  au- 
<;       riculo  -  ventricular 
valves,  as  Hender- 
3       son  has  suggested ; 
E       for  this  second  ele- 
ment falls  in  early 
auricular  diastole. 
When  a  stream  of 
water     is     poured 
through   an   auric- 


Relation  of  Auricular  Systole  to  Heart  Sounds     r,i 

ulo-ventricular   orifice,   and   this   jet   is   abruptly   broken,   the 
valves  immediately  close.     The  sound  is  more  intense  when  the 
auricular  systole  falls  in  early  rather  than  in  late  ventricular 
diastole,  and  this  is  to  be  expected,  for  at  such  a  time  the  ventri- 
cle is  full  and  any  opening  of  the  valves  must  be  followed  by  a 
quick    return    to    the    closed   position.     In    heart-block,    as    a 
rule,  the  auricular  contraction  is  followed  by  a  single  sound, 
and   it   is   probably   brought   about   in   the   manner   to   which 
reference  has  just  been  made.     But   if  the  auricular  sound 
is  audible  in  heart-block,  why  is  it  not  in  the  normal  heart 
beat  ?     I  suggest  because  the  auricular  and  ventricular  systoles 
are  too  near  together.     Normally  the  end  of  auricular  systole 
is  terminated  sharply  by  ventricular  systole.     There  is  no  inter- 
systolic  period.     The  'swing  of  the  A-V  valves  which  is  to  be 
expected  at  the  cessation  of  auricular  contraction  would  coin- 
cide with  closure  and  tension  of  these  valves  as  a  result  of  ven- 
tricular systole.     Assuming  this  view  to  be  correct,  then  if  for 
any  reason  the  closure  of  the  A-V  valves  as  a  result  of  ventric- 
ular systole  were  delayed,  we  should  expect  double  closure  of 
the  valves;  the  first  resulting  from  the  wake  of  the  aurimhir 
systolic  blood;  and  after  a  short  pause  a  second  closure  result- 
ing from  ventricular  systole.     It  is  actually  the  experience  that 
when  the  As-Vs  interval  is  prolonged,  a  double  sound  is  often 
audible,  for  it  is  in  these  cases  a  fortiori  that  gallop  rhythm 
appears.     It  is  also  frequently  present  in  those  curious  cases 
in  which  the  excitation  wave  appears  to  take  an  abnormal  course 
through  the  ventricular  walls.     Gallop  or  canter  rhythm  is  of 
two  kinds ;  in  the  commonest  type  the  additional  sound  happens 
immediately  before  the  natural  1st  heart  sound;  in  the  second 
type,  the   additional  sound  lies  in  early  or  mid-diastole.      A 
beautiful  example  of  the  first  variety  is  seen  in  Fig.  50.     That 
.    the  first  element  of  the  canter  lies  in  presystole  is  quite  clear  in 
this  record;  it  is  equally  clear  that  it  lies  toward  the  termina- 
tion of  auricular  svstole,  the  As-Vs  interval  being  a  little  pro- 


62 


Chapter  III 


longed.  If  we  examine  this  curve  in  detail  and  focus  our  at- 
tention upon  the  composite  sound,  what  strikes  us  most  is  the 
similarity  of  its  two  elements.  The  likeness  is  so  perfect  as  to 
convince  us  that  both  elements  have  a  common  origin ;  the  2nd 


Fig.  50.     Canter  rhythm  at  the  apex  beat;   from  a  patient  who  presented 
evidence  of  a  right  bundle  branch  defect. 

element  must  be  attributed  to  ventricular  systole.  The  1st 
cannot  be  so  explained,  for  it  begins  outside  the  bounds  of  sys- 
tole; but  both  elements  may  be  assigned  to  closure  of  the  A-V 
valves,  the  first  produced  by  the  termination  of  auricular,  the 
second  by  the  onset  of  ventricular,  systole,  in  the  manner  al- 
ready indicated.  It  is  also  to  be  remarked  that  in  no  instance 
as  yet  has  a  reduplication  of  this  kind  been  seen  where  the 
auricles  are  in  the  state  of  inactivity  associated  with  fibrilla- 
tion; it  has  always  been  associated  with  a  natural  sequence  of 
contractions,  but  as  a  rule  with  a  sequence  somewhat  delayed 
by  the  interposition  of  an  intersystolic  interval.  Examples  in 
which  there  is  no  delay  in  sequence  are  to  be  seen  in  Figs.  51 
and  52.  In  these  the  additional  sound  falls  with  the  begin- 
ning or  height  of  auricular  contraction  and  is  perhaps  com- 


- 


Relation  of  Auricular  Systole  to  Heart  Sounds     63 


/          3EE  / 


Fig.  51 


Fig.  52. 

parable  to  the  1st  auricular  element  of  Fig.  49.  It  may  be 
that  in  such  cases  we  have  to  deal  with  hypertrophy  of  the 
auricle.  In  Fig.  53  the  extra  sound  is  in  mid-diastole  and 
here  the  height  of  auricular  contraction  falls  immediately  after 
and  upon  the  end  of  the  preceding  ventricular  systole ;  in  all 


64  Chapter  111 

probability,  the  sound  has  been  produced,  or  at  the  least  has  been 
enhanced,  by  the  auricular  contraction. 


,£~±L 


Fig.  53. 

Fig.  51,  52,  and  53.     Examples  of  canter  rhythm;  the  extra  sound  accom- 
panying auricular  contraction. 


790 


Fig.  54.     Canter  rhythm;  the  extra  sound  falling  in  early  diastole. 

What  appears  to  be  wide  reduplication  of  the  second  sound 
is  seen  in  Fig.  54 ;  here  diastole  is  long  and  there  is  no  ques- 


Relation  of  Auricular  Systole  to  Heart  Sounds     65 

tion  of  auricular  systole  taking  part,  for  the  sound  is  far  re- 
moved from  it.  Similar  apparent  reduplications  are  seen  in 
Figs.  55  and  56,  in  both  of  which  the  auricles  are  fibrillating. 


'/ZQ 


Fig.   55   and   56.     'Canter   rhythms   in   cases   of   auricular   fibrillation;    the 
extra  sound  being  related  to  early  diastolic  events. 

This  type  of  canter  rhythm  is  very  evidently  of  different  origin 
to  the  first.  It  is  not  to  be  ascribed  to  asynchronous  closure  of 
the  semilunar  valves,  for  in  all  the  figured  instances  the  sounds 


66  Chapter  III 

were  of  maximal  intensity  near  the  apex  or  the  canter  was- 
confined  to  this  region;  and  also  because  the  elements  stand 
too  far  apart  from  each  other.  In  simple  reduplication  which 
may  be  ascribed  to  asynchronous  semilunar  closure,  the  two  ele- 
ments are  fused  and  are  scarcely  distinguishable  in  records. 
The  3rd  sound  (the  2nd  element  of  the  reduplication)  is  du& 
to  some  event  occurring  a  little  while  after  the  A-V  valves  open 
in  early  diastole;  it  may  be  that  these  valves  are  set  in  vibra- 
tion by  quick  filling  of  the  ventricle  and  their  consequent  clos- 
ure, in  given  cases,  as  Thayer  and  Hirschfelder  have  sug- 
gested in  describing  the  third  sound  of  the  normal  heart  beat. 
Many  of  the  instances  which  I  show  you  are  almost  certainly 
exaggerations  of  this  extra  sound  which  may  be  heard  in 
healthy  subjects. 

I  leave  the  question  of  canter  rhythm,  fully  aware  that  the 
description  is  incomplete,  but  content  if  I  have  satisfied  you 
that,  in  some  instances  at  all  events,  auricular  contraction  may 
be  responsible  for  it  and  that  we  have  still  much  to  learn  by 
careful  study  and  the  use  of  the  graphic  method. 

Some  little  while  since  a  curious  change  in  the  heart  sounds 
was  described  by  Dr.  Griffith  of  Manchester  in  cases  of  com- 
plete heart-block.  It  transpires  not  only  that  the  auricular 
sounds  are  audible  in  this  disorder  of  the  heart  beat,  but  that 
the  incidence  of  auricular  contractions  profoundly  affects 
the  quality  and  amplitude  of  the  ventricular  sounds.  The 
variation  is  such  that  it  forms  a  most  valuable  bedside  test 
of  complete  heart-block  when  instrumental  aids  are  not  avail-  „ 
able.  As  Griffith  described  it,  it  consists  of  a  great  increase  in 
the  loudness  of  the  1st  heart  sound  when  an  auricular  contrac- 
tion falls  synchronously  with  the  beginning  of  ventricular 
systole.  The  phenomenon  is  clearly  to  be  seen  in  Fig.  57  and 
you  will  notice  that  the  intensification  comes  when  the  auricular 
contraction  slightly  precedes  the  ventricular;  if  the  relation- 
ship is  reversed,  as  in  the  first  cycle  of  this  figure,  the  1st  sound 


Relation  of  Auricular  Systole  to  Heart  Sounds     67 

tends  to  reduplicate.  A  gradual  change  of  intensity  as  the 
auricular  systole  gradually  moves  over  the  commencement  of 
ventricular  systole  is  seen  in  Fig.  58.  All  these  1st  sounds  are 
greatly  accentuated  but  that  of  the  first  cycle  especially  so. 
The  figure  should  be  compared  with  Fig.  49  which  is  from  the 
same  case  and  taken  at  the  same  sitting.  The  complete  physical 
sign,  as  you  may  hear  it  in  almost  any  case  of  total  dissocia- 


' 


T 


4=5 


Fig.  57.     From  a  case  of  complete  heart-block;    showing  the  accentuation 
of  the  1st  sound  when  the  auricular  sj-stole  overlaps  the  ventricular. 

tion,  when  the  pulse  is  regular,  consists  of  an  accentuated  1st 
heart  sound  occurring  in  a  periodic  fashion  and  associated  also 
with  periodic  reduplication  of  both  1st  and  2nd  sounds.  Such 
variation  of  the  sounds  is  very  striking ;  it  occurs  so  far  as  I  am 
aware  in  no  other  condition,  being  distinctive  of  A-V  dissocia- 
tion. 

Mitral  stenosis. 

For  the  remaining  time  I  propose  to  discuss  the  murmurs  of 
mitral  stenosis  and  their  relation  to  events  in  the  auricle.  Let 
us  consider  in  the  first  instance  the  characteristic  murmur  of 
mitral  stenosis  which  accompanies  a  regular  heart  action. 


68 


Chapter  HI 


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Relation  of  Auricular  Systole  to  Heart  Sounds     69 


Fig.  59,  60,  and  61.     Examples  of  apical  murmurs  in  three  cases  of  mitral 

stenosis. 


70  Chapter  III 

Called  presystolic  by  almost  universal  custom,  it  is  generally 
believed  to  be  presystolic  in  time ;  yet  as  you  are  aware  its 
actual  position  in  the  cardiac  cycle  has  been  hotly  contested  on 
many  occasions.  Ormerod,  Barclay,  Dickinson,  and  lastly 
Brockbank  have  held  it  to  be  in  reality  systolic.  The  final 
proof  of  its  presystolic  position  has  been  supplied  by  graphic 
records.  Even  when  it  has  a  duration  of  no  more  than  l-20th 
or  l-30th  of  a  second,  it  comes  before  the  beginning  of  the  1st 
sound.  Gairdner  called  it  the  auriculo-systolic  murmur,  and 
his  suggestion  that  it  results  from  auricular  systole  is  almost 
certainly  correct  in  the  main;  though  this  statement  requires 
some  amplification.  In  most  cases  of  considerable  stenosis 
where  the  heart's  action  is  regular,  for  example  in  such  cases 
as  come  to  us  in  an  out-patient  department,  the  murmur  usually 
occupies  the  whole  diastole.  This  filling  of  diastole  is  due  to 
the  fact  that  there  is  generally  some  acceleration  .of  the  heart 
and  the  diastole  is  therefore  short.  Many  murmurs  commonly 
called  presystolic  in  reality  occupy  the  whole  of  diastole  as 
graphic  records  show  quite  clearly  (Fig.  59).  They  lie  in  pre- 
systole,  it  is  true,  but  also  in  mid-  and  early  diastole.  The  term 
presystolic  murmur  properly  speaking  should  be  confined  to  a 
murmur  isolated  in  presystole.  On  listening  to  heart  sounds 
at  the  apex  beat,  we  are  too  apt  to  time  murmurs  relative  to 
the  1st  sound  and  to  neglect  the  relation  to  the  2nd  heart  sound. 
I  think  too  that  a  murmur  is  often  called  presystolic,  not  be-" 
cause  it  is  so  timed,  but  because  it  has  the  rasping  and  rumbling 
qualities  which  are  usually  borne  by  such  murmurs.  Timing 
by  auscultation  is  often  a  difficult  or  impossible  task  if  it  is  to 
be  carried  out  with  any  pretension  to  accuracy.  At  all  events 
the  fact  remains  that  isolated  presystolic  murmurs  are  com- 
paratively rare ;  they  occur  when  the  heart  rate  is  slow  or  when 
the  stenosis  is  not  extreme;  an  example  is  to  be  seen  in  Fig.  62. 
Two  murmurs  of  the  same  quality  may  be  present,  the  one  in 
early  and  the  other  in  late  diastole ;  this  condition  is  seen  when 


Relation  of  Auricular  Systole  to  Heart  Sounds     71 

the  heart  rate  is  slow  and  the  stenosis  considerable.  Thus  the 
murmurs  which  accompany  mitral  stenosis  in  different  patients 
are  very  variable  in  their  time  relations ;  they  also  vary  greatly 
from  cycle  to  cycle  in  the  same  patient  and  vary  both  in  time 
.and  quality.  The  meaning  of  such  variations  will  be  discov- 
ered in  the  sequel.  The  murmurs  of  mitral  stenosis  have  the 
lowest  vibration  frequence  of  any.  The  frequence,  as  a  rule,  is 
the  same,  it  may  be  a  little  faster,  as  the  vibration  frequence 
•of  the  1st  sound  in  the  same  case.  The  similarity  of  frequence 
speaks  for  the  origin  of  the  murmur  in  vibration  of  the  mitral 
valve. 

If  we  consider  the  simplest  type  of  murmur,  that  which  falls 
in  presystole,  we  observe  that  it  is  related  to  auricular  systole ; 
the  murmur  commences  near  the  height  of  auricular  contraction 
(Fig.  62)  or  starting  earlier  is  reinforced  at  this  time  (Fig.  GO, 
3rd  cycle,  and  Fig.  61).  Such  at  any  rate  are  the  common 
events.  JSTo  one  will  doubt  I  think  that  the  murmurs  of  mitral 
stenosis  are  produced  by  the  passage  of  blood  from  auricle  to 
ventricle  through  a  constricted  orifice.  The  relations  of  the 
simpler  murmurs  suggest  that  the  propulsion  of  blood  by  auric- 
ular contraction  is  an  important  factor  in  their  production. 
In  some  cases  it  is  an  all  important  factor  and  in  these  we  may 
•correctly  call  the  murmur,  as  Gairdner  did,  auriculo-systolic. 
Figs.  62  and  63  were  taken  from  a  single  case  at  a  few  days 
interval.  In  the  first  curve  the  murmur  begins  at  the  height 
-of  auricular  systole,  and  lies  wholly  in  presystole.  This  curve 
was  taken  from  a  case  susceptible  to  the  influence  of  digitalis 
.and  by  administering  this  drug  it  was  possible  to  alter  the  rela- 
tion of  auricular  and  ventricular  systole.  The  influence  of 
auricular  systole  upon  the  murmurs  could  be  studied  therefore 
in  an  exact  manner.  After  the  administration  of  digitalis  the 
auricular  systole  lay,  not  in  presystole,  but  in  late  ventricular 
systole  and  early  diastole  (Fig.  63).  As  an  association  the 
murmur  altered  its  position,  leaving  presystole  and  appearing 


72 


Chapter  111 


T 


'k/Ul/ytfc 

•ffmpij 


Fig.  62  and  63.     Two  records  from  the  apex  beat  in  a  case  of  mitral  steno- 
sis, before  and  after  the  onset  of  partial  heart-block. 


Relation  of  Auricular  Systole  to  Heart  Sounds     73 

in  early  diastole ;  as  a  matter  of  fact  not  in  earliest  diastole,  but 
at  a  point  in  the  cycle  a  little  after  the  opening  of  the  A-V 
valves.*  The  influence  of  auricular  systole  upon  the  murmur 
in  this  case  can  hardly  be  questioned.  The  appearance  of  a 
gap  between  murmur  and  1st  sound  when  the  As-Vs  interval 
is  prolonged  was  first  reported  by  Galabin ;  it  has  been  empha- 
sised from  sounder  data  by  Mackenzie  in  recent  years.  I  would 
remind  you  too  that  Dr.  Cohn  of  Xew  York  has  reported  an 
instance  of  mitral  stenosis  in  which  2:1  heart-block  devel- 
oped as  a  result  of  digitalis  administration  and  that  when  the 
block  appeared  and  the  auricle  was  beating  at  twice  the  ven- 
tricular rate,  two  similar  murmurs  were  audible  in  each  dias- 
tole, one  in  mid-  and  the  other  in  late  diastole.  I  have  wit- 
nessed the  same  phenomenon  on  several  occasions  and  have  felt 
the  double  thrill  at  the  apex  in  diastole.  The  importance  of 
the  auricular  systole  in  influencing  these  murmurs  is  therefore 
beyond  doubt. 

Some  years  ago  an  extremely  important  observation  was  made 
by  Mackenzie ;  if  you  examine  the  earlier  papers  of  Galabin  and 
Fagge,  you  will  find  it  foreshadowed;  for  these  authors  noted 
the  disappearance  of  the  murmur  of  mitral  stenosis  when  the 
heart  becomes  irregular,,  or  its  isolation  in  early  diastole  when 
the  auricular  contraction  could  no  longer  be  recorded.  But  it 
is  to  Mackenzie's  exact  work  that  we  really  owe  our  chief  knowl- 
edge of  the  behaviour  of  murmurs  when  the  heart  beat  becomes 
disordered.  He  has  spoken  in  the  most  decided  manner  upon, 
the  subject,  and  has  stated  that  when  irregularity  of  the  ven- 
tricle^ which  we  now  know  to  be  attributable  to  fibrillation  of 
the  auricle,  becomes  established  in  a  case  of  mitral  stenosis,  the 
presystolic  murmur  vanishes,  and  its  disappearance  he  attrib- 
uted to  inactivity  of  the  auricles  during  diastole.  That  Mack- 

*  In  using  the  word  "  opening  "  one  refers,  in  a  case  of  mitral  stenosis, 
to  the  time  of  the  first  entry  of  blood  from  auricle  to  ventricle. 
f  Ascribed  by  Mackenzie  to  "  Nodal  rhythm.'' 


74  Chapter  III 

enzie's  statement  is  in  the  main  a  correct  one,  graphic  records 
proclaim.  I  may  briefly  describe  the  events  as  they  are  known 
to  us.  The  murmurs  of  mitral  stenosis,  when  the  auricles  are 
fibrillating,  are  peculiar ;  an  isolated  presystolic  murmur  is  not 
heard;  the  whole  diastole  may  be  filled  by  murmur  (Fig.  64), 


Fig.  64  and  65.     Two  apical  records  from  a  single  case  of  mitral  stenosis 
and  auricular  fibrillation,  before  and  after  treatment  with  digitalis. 

and  this  occurs  when  the  heart's  rate  is  rapid  and  the  stenosis 
is  great,  or  if  the  rate  is  slower  the  murmur  is  confined  to  early 
diastole.  The  commonest  condition  is  one  in  which  short  and 
long  diastoles  are  mixed;  and  in  which  the  former  are  filled 
by  murmurs,  while  in  the  longer  ones  the  murmur  tails  away 
and  vanishes  in  mid-  or  late  diastole  (Figs.  65  and  66). 


Relation  of  Auricular  Systole  to  Heart  Sounds     75 

The  important  point  to  notice  is  that  the  fixed  relation  is  to  the 
2nd  and  not  to  the  1st  heart  sound.  When  a  case  of  mitral 
stenosis  with  fibrillation  is  first  examined,  the  murmur  generally 
completely  fills  the  whole  diastole  (Figs.  64  and  67),  or  only 


<ko 

« »J  I  It 


/      *  n 


I*     T  I"   r 


?**  il 


Fig.  66  and  67.  Two  apical  records  from  cases  of  mitral  stenosis  with 
auricular  fibrillation.  In  Fig.  67,  the  diastolic  murmur  shows  nota- 
ble sub-divisions. 

fails  to  fill  a  very  occasional  diastole.  As  the  heart  slows  upon 
digitalis  (Fig.  65)  the  murmur  persists  but  now  tails  away  as 
diastole  proceeds.  A  gap  appears  between  it  and  the  next  1st 
sound,  and  the  length  of  this  gap  depends  upon  the  length  of  the 


T6 


Chapter  III 


particular  diastole.  The  difficulty  in  properly  timing  the  mur- 
mur lies  in  this  variability ;  in  reality  the  murmur  is  constantly 
early  diastolic,  but  in  some  cycles  it  is  curtailed  by  the  quickly 
succeeding  systole  of  the  ventricle;  in  others  its  full  develop- 
ment is  permitted,  while  in  others,  where  it  can  run  its  full 
course,  the  diastole  subsequently  proceeds  for  a  period  silently. 
When  I  speak  of  early  diastole,  I  should  perhaps  qualify  this 
term.  The  murmur  may  be  confined  to  early  diastole,  but 
more  often  it  is  in  delayed  early  diastole,  that  is  to  say,  there  is  a 
little  gap  between  2nd  sound  and  murmur.  Lastly,  there  may 
be  no  murmur  although  stenosis  of  slight  or  moderate  grade  is 
present ;  these  cases  are  quite  frequent. 

I  pass  to  a  further  discussion  of  the  causation  of  the  mur- 
murs and  especially  to  a  working  hypothesis  which  helps  us  to 
remember  and  to  explain  their  variations  under  different  con- 
ditions of  heart  action  etcetera.  First  of  all,  I  may  sum  up, 
making  the  chief  statements  in  regard  to  the  murmurs  of  mitral 
stenosis  in  tabular  form.  The  table  expresses  the  facts  in 
broad  outline. 


Heart 

Action    slow,    stenosis 
slight. 

Action    slow,    stenosis 
moderate. 

Action    slow,    stenosis 
considerable. 


Action  rapid,  stenosis 
slight. 

Action  rapid,  stenosis 
greater. 


Murmurs  of  Mitral  Stenosis. 

Normal  Rhythm  Auricular  Fibrillation 


Presystolic 

Presystolic,  perhaps 
also  delayed  early  dias- 
tolic. 

Presystolic  and  delayed 
early  diastolic,  or  full 
diastolic. 


Presystolic      or      more 
commonly  full  diastolic. 


Full  diastolic. 


No  murmur. 

No  murmur  or  delayed 
early  diastolic. 

Constant  delayed  early 
diastolic  with  full  dias- 
tolic for  shorter  dias- 
toles. 

No  murmur  or  more 
commonly  a  full  dias- 
tolic. 

Full  diastolic;  perhaps 
early  diastolic  only  in 
longest  diastoles. 


Relation  of  Auricular  Systole  to  Heart  Sounds     77 

It  will  be  seen  that  a  murmur  may  lie  in  presystole  while  the 
auricles  fibrillate ;  so  that  it  is  not  correct  to  say  that  a  murmur 
is  never  found  in  this  phase  of  the  cardiac  cycle  under  these 
conditions.  It  is  correct  to  state  that  an  isolated  presystolic 
murmur  is  not  found  as  an  accompaniment  of  fibrillation.  At 
all  events  this  statement  is  true  in  the  great  majority  of  cases 
and  at  the  most  has  exceptions  in  occasional  single  cycles  in 
rare  cases.  If  we  scan  .the  two  columns  of  our  table  we  re- 
mark that  the  murmurs  accompanying  the  normal  rhythm  and 
those  which  accompany  fibrillation  differ  only  in  one  important 
respect;  in  fibrillation,  as  we  might  anticipate,  such  mur- 
murs as  may  be  attributed  to  auricular  systole  are  not  present. 
If  this  chief  feature  is  remembered,  and  it  is  also  remembered 
that  the  murmurs  are  less  intense  when  the  heart  is  failing  and 
engorged,  and  that  such  engorgement  is  more  apt  to  occur  as  an 
accompaniment  of  fibrillation  than  as  an  accompaniment  of  the 
normal  rhythm,  then  the  arrangement  of  the  murmurs  should 
be  clear.  How  in  a  given  case  may  the  variations  be  explained  ? 
In  the  first  two  lines  of  Fig.  68  is  a  diagrammatic  representa- 
tion of  simultaneous  intra-auricular  and  intra-ventricular  pres- 
sures. In  the  third  line  I  have  represented  the  differences  in 
pressure  between  the  two  chambers.  When  the  semilunar 
valves  close  (S.C.  line)  the  pressure  in  the  ventricles  is  still  far 
above  that  in  the  auricles;  the  ventricular  pressure  is  falling 
while  the  pressure  in  the  auricle  is  rising  for  the  blood  is  col- 
lecting in  it.  There  comes  a  point  when  the  auricular  pressure 
exceeds  the  ventricular  (A-V-0  line)  and  at  this  point  the  A-V 
valves  open,  and  the  filling  of  the  ventricle  begins.  The  filling 
continues  but  gradually  falls  off  in  rate  as  it  proceeds,  for  the 
pressure  in  the  ventricle  is  rising,  until  at  the  end  of  diastole, 
and  with  the  systole  of  the  auricle,  the  auricular  pressure  rises 
suddenly  and  the  filling  is  again  hurried.  In  the  normal  heart 
cycle  there  are  two  periods  of  diastole  during  which  filling  is 
most  rapid ;  these  are  the  periods  at  which  the  differential  pres- 


78  Chapter  III 

sure  is  greatest  on  the  auricular  side;  these  are  the  periods  at 
which  the  murmurs  of  stenosis  are  to  be  anticipated,  for  the 
murmurs  are  controlled  by  the  rate  at  which  the  blood  flows 
through  the  narrowed  mitral  orifice.  I  suggest  that  the  pres- 


Mivt- 


\ 


Fig.  68.     A  diagram  of  intracardiac  pressures,  to  illustrate  the  influence 
of  such  pressures  upon  the  murmurs  of  mitral  stenosis. 

ence  or  absence  of  a  murmur  is  dependent  upon  the  presence  or 
absence  of  a  critical  rate  of  blood  flow.  In  some  cases  the 
necessary  rate  is  only  reached  in  presystole.  These  are  cases 
where  filling  is  on  the  average  slow,  where  the  stenosis  is  slight 
and  the  auricles  are  active.  If  the  stenosis  is  greater,  the 
average  rate  of  filling  increases,  so  it  does  also  if  the  heart  rate 
increases,  for  this  curtails  diastole.  As  the  average  rate  of 
filling  increases,  so  the  murmurs  will  become  more  manifest, 
and  will  appear  not  only  in  presystole,  but  at  the  period  of 
next  most  rapid  filling,  namely,  at  the  opening  of  the  A-V 
valves.  As  the  rate  of  filling  becomes  still  faster  the  whole 
diastole  will  be  noisy.  In  fibrillation  cases  the  filling  will  occur 


Relation  of  Auricular  Systole  to  Heart  Sounds     79 

most  rapidly  at  first ;  therefore  the  murmurs  will  be  loudest  in 
early  diastole  and,  where  diastole  is  long  or  stenosis  moderate, 
may  be  confined  to  this  period.  This  hypothesis  sufficiently 
explains  our  observations ;  it  also  accounts  for  differences  in  the 
lengths  and  characters  of  the  murmurs  from  one  cycle  to  the 
next  in  a  given  case;  the  rate  of  filling  varies  with  different 
phases  of  respiration,  etc. ;  the  hypothesis  also  accounts  for 
variations  in  the  murmurs  in  a  given  patient  from  day  to  day, 
for  the  blood  flow  varies  in  average  rate,  and  the  differential 
pressure  curve  varies  in  character  from  time  to  time  and  in 
different  circumstances. 

KEFEKENCES 

Brockbank.     "  The  murmurs  of  mitral  disease."     Edin.  and  Lond., 

1899. 

Cohn.     Brit.  med.  Journ.,  1909,  II,  1153. 
Einthoven.     Archiv.  Neerland.  d.  Sci.   exact,   et  nat.,  La  Haye, 

1907,  ser.  2,  XII,  401. 

Einthoven,  Archiv.  f.  d.  ges.  Physiol,  1907,  CXVII,  461. 
Fagge.     Guys?  Hosp.  Rep.,  1871,  3rd  ser.,  XVI,  247. 
Fahr.     Heart,  1912-13,  IV,  147. 
Gairdner.     Edin.  med.  Journ.,  1861-2,  VII,  438. 
Galabin.     Guys'  Hosp.  Rep.,  1875,  3rd  ser.,  XX,  282. 
Gibson.     Lancet,  1907,  II,  1380. 
Griffith.     Heart,  1911-12,  III,  143. 
Lewis.     Heart,  1912-13,  IV,  241;  Quart.  Journ.  of  Ned.,  1913, 

VI,  441. 
Mackenzie.     Brit.  med.  Journ.,  1904,  I,   529  and  1905,  I,  759; 

Quart.  Journ.  of  Med.,  1807-8,  I,  39." 
Thayer.     Archiv.  of  internal  Med.,  1909,  IV,  297,  etc. 
Weiss  and  Joachim.     Archiv.  f.  d.  ges.  Physiol,  1908,  CXXIII, 

341. 


CHAPTER  IV 

THIRD    HERTER    LECTUKE 

OBSERVATIONS  UPON  DYSPNCEA,  WITH  ESPECIAL 
REFERENCE  TO  ACIDOSIS 

Gentlemen, 

In  my  first  two  lectures  I  have  considered  two  subjects,  elec- 
trocardiography  and  phonography,  using  them  to  illustrate  the 
value  of  precise  laboratory  methods  in  clinical  observation. 
The  third  illustration,  which  forms  our  present  topic,  carries 
us  farther  afield.  I  propose  to  speak  of  certain  recent  observa- 
tions upon  dyspnoea,  touching  upon  questions  of  chemical 
pathology. 

The  application  of  chemical  pathology  to  clinical  problems 
has  been  and  still  is  sadly  neglected.  In  the  very  near  future 
this  branch  of  medical  science  will  be  one  of  our  greatest  assets. 
I  look  forward  to  a  time  when  no  large  institute  for  the  treat- 
ment of  patients  will  remain  unprovided  with  a  fully  equipped 
chemical  laboratory,  controlled  by  skilled  analysts;  to  a  time 
when  such  a  department  will  be  deemed  as  indispensable  as 
that  of  bacteriology.  We  can  afford  to  neglect  no  channel  of 
approach  in  studying  the  problems  of  disease.  We  must  pre- 
pare for  these  innovations  in  method.  If  it  is  said  that  the 
simple  bedside  tests  are  of  first  importance  to  the  practitioner, 
for  these  are  alone  available  to  him  in  his  routine  work,  it  may 
be  replied  that  the  laboratory  and  skilled  assistance  may  be 
brought  permanently  within  his  reach.  It  is  not  and  never  can 
be  wholly  a  question  of  facility ;  it  must  eventually  be  a  ques- 
tion of  the  comparative  merits  of  one  or  other  method.  Our 
conceptions  of  health  and  disease  are  the  foundations  upon 
which  the  happiness  of  the  human  race  rests.  Our  present 

81 


82  Chapter  IV 

expenditure  in  the  advancement  of  medicine  by  research  is  as 
nothing  to  our  outlay  upon  national  and  commercial  enterprises. 

Let  me  commence  my  present  illustration  by  relating  how 
my  interest  was  first  awakened  in  the  chemistry  of  dyspnoea. 
It  was  by  remarking  upon  the  strange  disproportion  between 
cyanosis  and  breathlessness  in  given  cases.  Bring  to  mind 
those  cases  of  congenital  heart  affection  or  of  mitral  stenosis  in 
young  people  in  which  cyanosis  is  a  most  conspicuous  feature ; 
such  patients  may  exhibit  little  breathlessness  while  they  rest. 
Yet  the  oxygenation  of  the  blood  is  evidently  grossly  deficient. 
Even  deep  cyanosis  may  be  present  while  the  respiratory  rate 
is  but  little  increased,  the  respiratory  reserve  but  partially  im- 
paired. "From  this  observation  it  may  be  argued  that  to  pro- 
duce urgent  dyspnoea,  the  lack  of  oxygen,  expressed  clinically 
as  cyanosis,  must  be  extreme.  Or,  put  from  the  other  point  of 
view,  if  dyspnoea  be  present  and  cyanosis  absent,  or  if  the 
cyanosis  be  not  of  equivalent  grade,  the  dyspnoea  is  due  wholly 
or  partially  to  a  cause  other  than  deficient  aeration  of  the  blood. 

Apply  this  argument  clinically  and  I  think  you  will  be 
forced  as  I  was  forced  to  the  view  that  a  very  large  proportion 
of  those  patients  who  exhibit  moderate  or  great  distress  of 
breathing,  while  they  lie  at  rest  in  bed,  are  suffering  from 
breathlessness  which  is  due  to  causes  other  than  lack  of  oxygen ; 
the  dyspnoea  comes  neither  from  an  obstruction  of  the  respira- 
tory passages  nor  from  defective  circulation  of  the  blood 
through  the  lungs.  To  what  then  is  it  due  ?  In  seeking  an 
answer  to  this  question,  I  requested,  and  was  fortunate  in 
securing  the  help  of  my  friend,  Mr.  Barcroft,  who  has  de- 
voted many  years  of  his  life  to  laboratory  researches  upon  gase- 
ous exchange  in  the  blood.  Such  results  as  I  am  able  to  relate 
are  due  to  his  collaboration,  for  the  chief  analytical  work,  the 
major  task,  has  fallen  to  his  share. 

As  the  sequel  will  show,  the  dyspnoea  described  results  from 
non-volatile  acids  in  the  blood.  The  method  employed  for  the 


Observations  Upon  Dyspnoea  83 

detection  of  this  increased  acidity  is  a  simple  one  and  consists 
in  estimating  the  degree  of  saturation  of  the  blood  with  oxygen, 
when  it  is  exposed  to  this  gas  at  a  known  pressure  and  under 
given  conditions.  For,  as  Barcroft  and  his  collaborators  have 
shown,  the  combination  of  haemoglobin  with  oxygen  is  mate- 
rially influenced  by  the  addition  of  minute  quantities  of  acid 
or  alkali.  Acid  diminishes,  alkali  increases  the  power  of  y 
haemoglobin  to  take  up  oxygen  when  it  is  exposed  to  this  gas.  | 
Barcroft  exposes  to  a  definite  pressure  of  oxygen  a  sample  of 
whipped  blood;  the  test  is  a  delicate  one;  if  the  quantity  of 
oxygen  absorbed  is  known,  the  amount  of  acid  which  must  be 
added  to  normal  blood  to  produce  a  similar  reaction  may  be 
calculated  in  percentage  terms.  If  the  same  blood  is  exposed 
to  oxygen  in  the  presence  of  CO2  at  tensions  equivalent  to  those 
found  in  the  alveolar  air  of  the  patient  from  whom  the  blood 
is  taken,  the  amount  of  oxygen  absorbed  gives  a  measure  of 
the  reaction  of  the  blood  as  it  circulates  in  the  patient.  The 
merits  of  this  method  are  recognised  by  those  who  are  in  a  posi- 
tion to  judge  of  them.  We  may  judge  them  ourselves  by  the 
results  which  are  yielded.  Mr.  Barcroft  working  at  Cambridge 
is  able  to  calculate  with  remarkable  accuracy,  by  examination 
of  samples  sent  to  him,  the  state  of  the  respiration  in  patients 
whom  he  has  never  seen,  patients  bedded  at  our  hospital  in 
London. 

It  will  be  convenient  to  speak  in  the  first  instance  of  patients 
who  have  signs  of  cardiac  disease.  The  observations  have 
clearly  shown  that  from  such  patients  a  distinct  and  large  group 
may  be  separated  at  once,  and  that  in  this  group  the  dyspnoea 
is  associated  with  the  presence  of  a  non-volatile  acid  in  the 
blood.  The  group  consists  of  patients  to  whom  I  have  already 
referred,  where  the  degree  of  cyanosis  is  disproportioned  to 
the  respiratory  distress.  Before  proceeding  to  a  detailed  state- 
ment of  the  symptom  complex,  we  may  briefly  discuss  the  ef- 
fects of  blood  reaction  upon  the  respiratory  centre.  The  blood 


84  Chapter  IV 

as  you  know  is  alkaline,  it  is  always  alkaline  whether  there  is 
health  or  disease.  When  we  speak  of  acidosis,  we  simply  mean 
that  the  blood  has  a  reduced  alkalinity.  Observation  goes  to 
show  a  remarkable  sensitivity  of  the  respiratory  centre  to  vari- 
ations in  the  blood  reaction;  so  sensitive  is  it  that  it  will  re- 
spond to  changes  of  reaction  which  are  far  beyond  our  most 
delicate  titration  tests.  It  has  been  shown  that  the  introduc- 
tion of  very  small  quantities  of  acid  or  acid  salt  int^ijfcfclood 
stream  is  followed  by  hyperpncea  (Leymann,  etc.),  ancMpft  the 
introduction  of  alkali  produces  apno3a.  It  is  immaterial  what 
the  acid  is ;  carbon  dioxide  acts  in  similar  fashion  to  mineral  or 
organic  acid.  Each  produces  its  effect,  according  to  the  modern 
view,  by  increasing  the  number  of  free  hydrogen  ions  in  the 
blood.  The  response  of  the  respiratory  centre  to  blood  reaction 
is  the  key  to  a  clearer  understanding  of  clinical  dyspnoea. 
Dyspnoea  resulting  from  increased  hydrogen-ion  concentration  is 
of  two  kinds,  it  may  come  from  volatile  or  non-volatile  acids. 

Simple  mechanical  dyspnoea. 

If  we  examine  relatively  simple  forms  of  cardiac  disease,  for 
example  the  mitral  stenosis  of  young  rheumatic  girls,  we  find 
that  such  dyspnoea  as  is  present  may  be  accounted  for  by  lack 
of  oxygen  and  accumulation  of  CO2 ;  for  the  alveolar  air,  which 
samples  the  gases  of  the  pulmonary  capillaries,  is  deficient  in 
oxygen  and  surcharged  with  CO2  in  these  cases.  Blood  taken 
from  these  patients  and  freed  from  CO2  has  a  normal  alkalinity ; 
there  is  no  excess  of  non-volatile  acid.  The  simplest  form  of 
cardiac  dyspnoea  is  caused,  therefore,  by  mechanical  defect,  an 
embarrassment  of  the  circulation  in  the  lungs.  As  a  general 
rule  such  dyspnoea  is  not  severe  in  patients  who  have  been  resting 
in  bed ;  if  cardiac  patients  continue  to  show  great  breathlessness 
another  factor  is  generally  discovered.  Dyspnoea  which  comes 
from  mechanical  causes,  be  they  primarily  of  circulatory,  pul- 
monary or  bronchial  origin,  proclaims  itself  clinically  .by  its 


Observations  Upon  Dyspncea  85 

attendant  cyanosis.  In  cardiac  patients  who  have  this  simple 
mechanical  dyspnoea,  venous  and  liver  engorgement  are  the  rule ; 
such  patients  prefer  to  sit  than  to  lie,  for  while  lying  the  passage 
of  venous  blood  from  abdomen  to  heart  is  encouraged  and  the 
patients  are,  as  a  consequence,  orthopnoeic.  If  in  these  patients, 
you  press  upon  the  abdomen,  the  respiratory  rate  and  volume  at 
once  become  increased  (Fig.  69).  The  same  patients  may  com- 


Fig.  69.  A  curve  of  respiration  in  a  patient  suffering  from  simple  car- 
diac dyspnoea,  showing  the  increase  in  the  rate  and  depth  of  ventila- 
tion upon  compressing  the  abdomen. 

plain  of  aggravated  breathlessness,  which  at  night  wakes  them 
from  sleep.  This  form  of  nocturnal  breathlessness  is  to  be 
clearly  distinguished  from  a  variety  which  I  shall  presently 
^describe;  it  is  due  to  the  patients  slipping  down  the  bed  from 
;ofi>their  pillows. 

^The  respiratory  excursion  is  irregular  in  amplitude  and  in 
rhythm ;  reserve  is  reduced,  so  that  the  breath  can  be  held  but 
for  a  few  seconds ;  forced  breathing  is  followed  not  by  apnosa  as 
in  the  normal  subject  but  by  a  resumption  of  the  previous  type 
of  breathing  or  even  by  increased  ventilation.  Great  distress 
is  rarely  witnessed  in  these  relatively  simple  cases. 

A  special  symptom  complex. 

The  facts  which  I  have  just  related  will  be  familiar  to  you. 
This  simple  cardiac  dyspnoea,  in  which  the  blood  circulating 
through  the  brain  is  overladen  with  CO2  is  not  difficult  to  recog- 
nise in  frank  cases.  Neither  is  the  second  type,  to  which  I 


Chapter  IV 


now  pass,  once  you  are  acquainted  with  the  clinical  picture.     1 

take  first  of  all  the  most  sim- 
ple examples.  There  are 
patients,  usually  elderly,  who 
are  admitted  to  our  wards 
and  suffer  from  urgent 
dyspnoea.  The  breathing  is 
laboured;  it  is  periodic  and 
of  the  Cheyne-Stokes  type 
(Fig.  70).  The  patients  are 
not  orthopnceic,  they  exhibit 
few  signs  of  venous  or  liver 
engorgement,  pressure  upon 
the  abdomen  does  not  materi- 
ally  increase  the  depth  or 
rate  of  respiration  (Fig.  71). 
The  uncomplicated  cases  are 
not  cyanosed.  The  blood  is  \ 
fully  aerated  and  has  a  low  l|f 


tension  of  CO2.  There  is 
little  or  no  reserve.  The  ad- 
ministration of  oxygen  af- 
fords practically  no  relief. 
A  conspicuous  feature  is  the 
presence  of  nocturnal  attacks 
of  breathlessness,  and  these 
wake  the  patients  repeatedly 
from  slumber,  are  often  suf- 
focative  and  last  from  a  few 
minutes  to  half  an  hour  or 
more.  The  heart  is  a  little 
dilated;  the  pulse  rate  is  al- 
most always  increased  (80- 
100)  and  especially  towards 


Observations  Upon  Dyspnoea  87 

evening.  The  temperature  is  generally  subnormal.  The  blood 
after  removal  of  its  CO2  shows  a  considerable  decrease  of  alka- 
linity, which  is  due  to  the  excessive  presence  of  non-volatile 
acids  or  acid  salts. 


Fig.  71.  A  curve  of  respiration  in  a  patient  suffering  from  slight  non- 
volatile acidosis.  Pressure  upon  the  abdomen  does  not  increase  the 
respirations  in  rate  or  depth. 

These  are  the  almost  constant  clinical  manifestations,  but 
the  picture  is  varied  in  a  hundred  ways.  Add  to  it  the  symp- 
toms and  signs  of  heart  disease  in  its  various  forms ;  add  to  it 
the  symptoms  and  signs  of  renal  disease  and  its  complications, 
add  emphysema,  or  cerebral  arterial  disease,  and  you  are  able 
to  reconstruct  the  protean  types  in  which  this  curious  acidosis 
is  displayed.  It  may  be  that  you  will  declare  the  special 
symptom  complex  which  I  describe  to  you  as  ursemic,  that  may 
or  may  not  be  justified;  I  have  deliberately  avoided  this  term 
on  account  of  its  laxity.  There  is  of  course  no  question  but  that 
many  of  the  cases  which  I  have  in  mind  are  commonly  termed 
ursemic;  for  the  urine  is  of  low  specific  gravity  and  contains 
albumen  and  granular  casts;  the  blood  pressure  is  often  high; 
and  other  so-called  "  ursemic  manifestations  "  frequently  appear. 
Severe  headache,  twitching  of  the  limbs,  vomiting,  temporary 
hemiplegia,  convulsive  seizures  or  aphasia  may  appear.  Thirst 
and  anorexia  are  common ;  wasting  and  a  little  anaemia  are  fre- 
quent ;  inflammatory  affections  of  lung  and  pleura  are  frequent 
terminal  complications.  But  what  I  wish  to  impress  is  that 
none  of  these  last  named  symptoms  is  essential  to  the  complex, 
any  more  than  are  those  cardiac  symptoms  which  I  shall  pres- 


88  Chapter  IV 

ently  describe  essential.  Ursemic  dyspnoea  is  a  term  which  we 
should  carefully  avoid,  for  it  presupposes  that  the  breathless- 
ness  is  primarily  of  renal  origin ;  of  this  we  are  not  certain  at 
the  present  time.  The  malady  and  its  varieties  can  only  be 
appreciated  fully  if  the  essential  features  are  isolated  or  con- 
stantly maintained  in  relief.  They  are  those  I  have  already 
enumerated,  and  which  I  now  repeat,  namely,  dyspnoea  in  the 
absence  of  cyanosis  or  an  equivalent  cyanosis,  accompanied  by 
periodicity  of  respiration  and  by  nocturnal  seizures ;  some  dila- 
tation of  the  heart,  rapid  pulse  action  and  a  subnormal  temper- 

i      ature.     Lastly,  there  are  the  characters  of  the  alveolar  air,  the    I  * 
high  oxygen  and  lovjj  CO2  content,  and  the  signs  of  a  non-vola- 
tile acid  in  the  blood. 

The  remaining  signs  and  symptoms  are  not  essential  features,, 
but  one  or  other,  or  several,,  are  almost  always  present.  The  un- 

^  complicated  case  is  rare.  It  is  to  this  fact  that  the  protean 
character  of  the  malady  is  due ;  it  is  to  this  fact  that  the  symptom 
complex  has  remained  hidden  in  the  past,  for  it  is  usually 
obscured  in  greater  or  lesser  degree.  Nothing  tends  to  hide  it 
more  than  the  presence  of  cardiac  failure,  and  this  is  an 
extremely  frequent  complication.  The  heart  may  be  affected 
in  a  variety  of  ways.  Any  valve  lesion  may  be  present,  aortic 
dilatation  or  actual  aneurysm  are  not  uncommon.  You  may 
find  all  varieties  of  altered  heart  mechanism ;  fibrillation  of  the 
auricles  and  pulsus  alternans  are  especially  frequent.  Anginal 
pains  may  be  present.  Engorgement  of  the  veins  and  liver, 
with  or  without  ascites  and  dropsy,  are  the  rule  rather  than  the 
exception  in  advanced  cases. 

These  superadded  phenomena  mask  an  otherwise  obvious  con- 
dition ;  engorgement  of  the  venous  system  especially  embarrasses 
the  diagnosis,  for  it  veils  or  hides  the  all  important  discrepancy 
between  the  breathlessness  and  the  oxygenation  of  the  blood. 
Many  of  these  unfortunate  people  suffer  not  only  from  a  fixed 
acidosis  but  in  addition  from  the  simple  form  of  cardiac 
dyspnoea,  due  to  lack  of  blood  aeration.  Generally  speak- 


Observations  Upon  Dyspnoea  89 

ing,  the  whole  trouble  of  breathing  is  referred  to  the  last  named 
cause;  for  where  the  pulmonary  circulation  is  evidently  defec- 
tive, where  in  the  presence  of  slight  or  moderate  cyanosis,  signs 
of  aneurysm,  of  emphysema,  or  of  venous  engorgement,  are 
found,  the  temptation  to  ascribe  the  whole  breathlessness  to  a 
purely  mechanical  cause  is  too  often  irresistible.  That  the 
mechanical  cause  is  not  the  sole  cause,  that  often  it  is  not  even 
the  chief  cause,  has  been  clearly  shown  by  the  blood  tests.  We 
become  more  and  more  convinced  as  these  tests  increase  in 
number  that  there  are  very  few  inmates  of  our  hospitals  who 
suffer  from  really  urgent  and  constant  breathlessness,  in  whom  a 
mechanical  hypothesis  is  sufficient  to  explain  the  symptoms. 
You  are  familiar  with  those  distressing  cases,  patients  of  mid- 
dle or  advanced  years,  who  in  a  semi-conscious  state,  sit  in 
chairs  in  our  wards,  and  while  cyanosed  and  dropsical,  struggle 
for  breath  during  the  rest  of  their  existences.  It  may  be  that 
mitral  stenosis,  it  may  be  that  aortic  disease  or  aneurysm  are 
present.  It  may  be  that  bronchitis  and  emphysema  are  diag- 
nosed. In  each  and  all  in  our  experience  a  non-volatile  acidosis 
is  a  chief  trouble.  The  more  we  see  of  the  blood  reactions,  the 
more  mechanical  dyspnoea  recedes  to  the  background.  The 
secret  of  the  clinical  diagnosis  lies  in  a  nice  discrimination 
between  the  degree  of  breathlessness  and  the  degree  of  cyanosis, 
in^a  menial  Comparison  between  these  patients  and  those  cases 
ol'TnTtral  stenosis  or^congenital  heart  disease  in  wiiicnthere 
is  an  obvTous^fackj^f  blood  Deration. 

Our  tests  show  quite  clearly  that  if  a  very  breathless  patient 
has  but  slight  or  moderate  cyanosis,  whether  or  no  such  patient 
is  afflicted  with  emphysema,  myocardial  or  valvular  heart  dis- 
ease, aneurysm  of  the  aortic  arch  or  what  not,  the  breathlessness 
cannot  be  ascribed  wholly  to  a  mechanical  cause.  In  the  light 
of  laboratory  observation  the  old  faiths  fall  away  fast.  Stronger 
and  stronger  becomes  the  conviction  that  death  from  actual  but 
gradual  asphyxia  in  an  uncomplicated  form  is  a  rare  event  in 


90  Chapter  IV 

our  patients,  and  that  by  far  the  commonest  form  of 'urgent 
breathlessness  is  the  acidosis  which  I  am  describing  to  you.  Go 
into  the  wards  of  a  general  hospital ;  you  will  rarely  fail  to  see 
a  number  of  sufferers  sitting  in  bed  and  in  urgent  need  of  breath ; 
three-fourths  at  least  of  such  cases  are  examples  of  the  condition 
now  considered. 

Their  diseases  are  partially  described  by  a  variety  of  diag- 
nosis; angina  pectoris,  aortic  disease,  aneurysm,  mitral  regur- 
gitation,  mitral  stenosis,  arterial  disease,  chronic  bronchitis, 
ursemia,  cardiac  asthma,  coronary  arterial  disease,  hydrothorax 
or  pleurisy.  In  each  and  all  of  these  conditions,  acidosis  may 
be  found  as  an  association,  when  the  laboratory  tests  are  un- 
dertaken. 

Where  the  breathlessness  is  due  to  non-volatile  acids  only, 
then  the  respiratory  embarrassment  is  proportioned  to  the 
degree  of  acidity.  When  such  patients  improve  the  acidity  is 
found  to  decline;  as  they  lose  their  breathlessness,  the  blood 
reaction  becomes  normal.  The  chemical  test  is  a  sensitive  lab- 
oratory indication  of  the  patients'  respiratory  exchange. 

Where  heart  failure  is  added,  then  the  breathlessness  is  gov- 
erned by  two  factors,  first  by  the  quantity  of  non-volatile  acid 
present,  and  secondly  by  the  degree  of  deficiency  in  aeration. 
The  two  combine  to  a  common  end,  the  creation  of  hyperpnoea. 
The  most  urgent  dyspnoeas  belong  to  this  group. 

It  is  also  to  be  noticed  that  the  presence  of  a  slight  grade  of 
relative  acidity,  although  it  may  not  in  itself  give  rise  to  promi- 
nent dyspnoea,  limits  the  reserve,  so  that  any  influence,  such  as 
exercise,  holding  the  breath,  etc.,  which  is  followed  by  increased 
ventilation  in  normal  subjects,  acts  in  these  subjects  with  exag- 
gerated effect.  The  field  of  respiratory  response  is  strictly 
limited  and  its  bounds  are  easily  crossed  by  these  people. 

Other  conditions  in  which  non-volatile  acidosis  has  been  found. 
I  have  sketched  for  you  the  type  of  case  where  you  may  most 


Observations  Upon  Dyspnoea  91 

readily  and  surely  find  the  acidosis  in  question.  There  are 
other  conditions  in  which  it  is  known  to  exist.  The  simplest 
example  is  physiological,  the  dyspnoea  of  violent  and  prolonged 
exercise  is  due  to  such  a  cause ;  here  too  there  is  no  cyanosis  and 
the  acid  responsible  has  proved  to  be  lacticacid,  formed  in  the 
contracting  muscles.  In  the  increased  ventilation  of  the  lungs 
of  diabetes,  the  alveolar  air  contains  more  oxygen  and  less  CO2 
than  normal.  The  hyperpncea  is  not  due  to  lack  of  oxygenation 
but  to  decreased  blood  alkalinity,  owing  to  the  presence  of 
oxybutyric  and  diacetic  acids.  On  account  of  this  relative 
acidity  the  respiratory  centre  is  stimulated,  ventilation  is 
increased,  the  CO2  in  the  blood  is  decreased,  oxygen  is  increased. 
In  this  manner,  a  partial  compensation  is  established.  But 
reserve  is  diminished.  A  similar  condition  is  discovered  in 
normal  subjects  at  high  altitudes,  though  the  nature  of  the  acid 
has  not  been  identified  as  yet.  In  two  of  the  patients  in  our 
own  series,  lactic  acid  was  found  in  excess  in  the  blood  by  Dr. 
Ryffel,  but  both  these  patients  wrere  at  the  time  moribund  and 
we  cannot  regard  it  as  the  invariable  or  even  the  common  male- 
factor ;  the  usual  acid  is  again  unknown., 

Recently  we  have  extended  our  search  amongst  clinical  cases 
and  have  found  a  similar  acidosis  in  a  number  of  conditions  in 
which  it  was  formerly  unsuspected.  These  observations  have 
not  been  published,  but  I  have  Mr.  Barcroft's  permission  to 
speak  of  them.  It  is  present  in  acute  lobar  pneumonia  and  is 
largely  responsible  for  the  dyspnoea  which  accompanies  this  con- 
solidation of  the  lung  tissue.  The  acidosis  may  be  of  high  grade, 
in  which  case  the  patients  in  our  experience  do  not  recover. 
Where  it  is  originally  of  slighter  grade,  it  persists  over  the  crisis 
to  vanish  hand  in  hand  with  the  breathlessness  as  the  patient 
becomes  convalescent.  In  view  of  these  facts,  we  are  no  longer 
justified  in  attributing  the  whole  breathlessness  of  pneumonia 
to  the  lung  damage ;  a  statement  which  is  supported  by  the  fact 
that  pneumococcal  lesions  in  other  parts  of  the  body  may  also 


Ckapter  IT 


be  associated  with  breathlessness.  We  have  recently  found  a 
acidosis  in  a  case  of  exophthalmic  goitre,  where  with 
taoe  symptoms,  such  as  vomiting  and  mania,  breathless- 
fas  distressing.  Xot  so  long  ago  a  patient  was  admitted  to 
having  developed  an  acute  pneumothorax,  a  secondary 
result  of  chronic  but  almost  quiescent  tuberculosis.  He  showed 
dyspnoea  which  varied  in  its  intensity ;  the  blood  reaction  pre- 
ariationsw  being  more  on  the  acid  side  while  the 
;  great,  and  more  on  the  alkaline  side  while  the  dysp- 
noea was  slight  or  ?^p^  This  instance  is  of  special  interest, 
for  with  unquestionable  signs  of  collapse  in  one  lung,  and  in  the 
absence  of  eheniieal  tests,  we  should  have  had  no  hesitation  in 
ascribing  the  respiratory  disturbance  to  a  mechanical  cause. 
Yet  die  chief  cause  was  not  mechanical  but  toxic.  Of  cases  of 
mitral  stenosis  in  early  years,  we  have  examined  a  number :  in 
all  but  one  of  these  patients  acidosis  was  absent.  The  solitary 
-  --• ::  :.  M  i  •  ••£  •  :...:..  i  priw-gnviaVi  •!  Ml  harm 
Here  acidosis  was  present  in  considerable  degree  and  granular 
casts  were  discovered  in  the  urine. 

Gentlemen,  the  observations  are  still  at  an  early  stage,  but 
they  are  full  of  promise.     There  is  in  fact  no  branch  of  clinical 
3y  of  which  I  know  which  offers  greater  opportunities  for 


workers  at  the  present  time.  There  is  a  wide  field  for 
The  requisite  laboratory  methods  are  at  our  disposal; 
we  have  but  to  apply  them  to  our  clinical  material  to  reap  a  rich 
harvest  of  new  facts.  One  conclusion  should  be  emphasised. 
We  are  not  justified  at  the  present  time  in  ascribing  dyspnoea 
to  a  mechanical  cause,  to  deficient  aeration  of  the  blood,  except 
in  the  most  simple  forms  of  cardiac  breathlessness,  or  where  an 
evident  obstruction  to  the  respiratory  passages  is  the  only  lesion 
in  the  patient.  !N  on-volatile  acids,  as  opposed  to  CO*,  appear  to 
be  an  almost  universal  cause.  There  seems  to  me  to  be  little 
doubt  that  aH  forms  of  so  called  renal  dyspnoea,  many  forms  of 

ilj  ujtnu  • ,  and  many  of  the  dyspnoeas  which  have  in  the 


Observations  Upon  Dyspmam 


past  been  ascribed  to  pressure  by  tumours,  such  as 
or  to  consolidation  of  the  lung,  collapse  or  emphysema  of  the 
same  organ,  are  produced  in  reality  mainly  through  the  product* 
of  altered  metabolism. 


;,-   i 

At  an  earlier  stage  I  described  in  some  detail  a  symptssft 
complex  in  elderly  subjects,  where  Cheyne-Stokes  breathing  and 
nocturnal  breathlessness  are  prominent  symptoms.     The  <J*t*- 
tion  as  to  whether  we  must  regard  such  breathlcMm  9m  «C 
renal  origin  in  these  patients  is  still  an  open  one.     All  presesrt 
signs  of  renal  involvement,  those  who  have  come  to  autopsy  have 
demonstrated  renal  lesions :  all  also  present  symptoms  of  cardiac 
affection.     Most  of  those  examined  after  death  disclose  coronary 
arterial   disease   and  a   degenerate  myocardium.     We  require 
analyses  in  cases  of  a  purer  kind ;  especially  we  require  investi- 
gation of  those  comparatively  rare  eases  of  dyspnoea  in  v 
subjects  where  the  kidneys  are  shrunken  and  pale.     A 
ease  of  parenchymatous  nephritis  is  included  in  our  series :  it 
a  man  who  died  with  universal  dropsy  of  frank  renal  type.     The 
acidosis  was  in  his  case  extreme  and  the  breathlessness  iciy 
urgent     A  most  suggestive  observation,  but  unhappily  not  un- 
complicated, for  at  autopsy  a  certain  grade  of  aortic  and  mitral 
mischief  was  also  discovered.     We  require  observations  upon 
pure   eclampsia   too  before   a   full   answer  ean   be   returned. 
Instances  of  breatnlessness  resulting  from  acidosis  in  patients 
described  as  uraemic  have  been  separately  and  recently 
by  Eyffel  and  Poulton.  but  their  description  and  the 
suggestion  that  the  dyspnoea  was  of  renal  origin  should  not  be 
accepted  before  we  have  full  clinical  details  of  their  eases :  the 
cases  which  they  describe  were  in  all  probability  of  the 
type  as  those  included  in  the  series  upon  which  my 
observations  are  based.     The  same  statement  applies  to  Straufe  U 
and  Schleyer's  patients  in  whom  a  decreased  CO;  content  was   | 


94  Chapter  IV 

discovered  in  the  alveolar  air.  This  change  in  constitution  of 
the  alveolar  air  was  rightly  regarded  by  them  as  evidence  of 
decreased  alkalinity  of  the  blood. 

Our  first  task  is  the  isolation  of  all  the  clinical  types  in  which 
dyspnoea  has  its  origin  in  acidosis.  It  were  wiser  in  investiga- 
tions of  this  kind  that  the  actual  facts  in  regard  to  the  patients 
observed  should  be  given  in  full  detail.  To  tabulate  the  cases 
under  such  broad  and  ill-defined  headings  as  uraemia  and  to  leave 
them  at  that  is  in  the  long  run  a  waste  of  valuable  material. 
That  uraemia  was  present  is  a  matter  of  opinion,  as  the  meaning 
of  a  term  which  still  lacks  definition  is  also  a  matter  of  opinion. 

The  second  task,  which  must  fall  purely  to  the  lot  of  the 
chemist,  is  the  identification  of  the  substance  or  substances 
responsible.  When  we  have  this  information,  we  shall  be  in  a 
position  to  investigate  and  discuss  the  seat  of  the  disorder,  and 
to  approach  its  treatment  with  greater  prospect  of  success.  At 
present  the  renal  origin  of  dyspnoea  is  chiefly  a  matter  of  specu- 
lation; therefore  I  do  not  propose  to  enter  further  upon  its 
discussion. 

Periodic  breathlessness. 

In  conclusion,  may  I  refer  to  certain  forms  of  periodic  breath- 
lessness.  Quite  recently  a  patient  came  to  my  out-patient 
department  for  an  examination  of  the  heart.  A  man  of  50 
years,  of  florid  appearance,  who  presented  signs  of  a  little  cardiac 
enlargement,  and  exhibited  upon  examination  some  very  slight 
breathlessness.  Other  physical  signs  were  few.  During  the 
course  of  his  examination,  he  became  abruptly  dyspnoeic  and 
within  a  few  moments  had  passed  into  a  condition  of  the  utmost 
gravity.  Breathlessness  was  the  primary  symptom,  the  respira- 
tory rate  rose  to  44  per  minute;  later  he  became  cyanosed, 
eventually  deeply  cyanosed,  the  temperature  fell  behnv  96°,  the 
pulse  increased  to  140,  the  expanded  chest  was  filled  with 


Observations  Upon  Dyspnoea  95 

rhonchi.  There  was  no  expectoration,  but  large  quantities  of 
urine  were  voided,  the  face  and  limbs  were  pale  and  cold,  the 
brow  clammy.  The  whole  attack,  lasting  but  a  few  hours,  gave 
rise  to  grave  anxiety  for  his  life.  A  sample  of  blood  taken 
during  the  attack  showed  a  profound  acidosis.  The  recover v 
was  almost  as  speedy  as  the  onset ;  and  samples  of  blood  exam- 
ined within  the  next  few  days  told  us  that  its  reaction  had 
returned  almost  to  normality.  The  attack  was  one  of  two  which 
the  patient  had  experienced.  Apparently  the  blood  had  of  a 
sudden  suffered  invasion  by  acid  products  in  sufficient  quantity 
to  bring  life  into  immediate  jeopardy.  What  was  the  cause  of 
this  flooding  of  the  system  ?  We  do  not  know.  Some  would 
call  it  an  attack  of  cardiac  or  renal  asthma ;  preferably  we  confine 
ourselves  to  the  known  fact  that  the  crisis  was  produced  by  the 
invasion  of  the  system  by  acid  products.  We  require  many 
more  observations  of  a  similar  kind,  we  require  them  not  only 
in  cases  suspected  of  renal  or  cardiac  disability,  but  in  every 
type  of  case  in  which  such  paroxysmal  seizures  are  to  be  found. 
It  may  or  may  not  be  that  there  is  a  condition  in  which  the 
bronchioles  become  suddenly  constricted,  the  old  bronchial 
asthma;  we  have  no  direct  proof,  though  we  have  strong  pre- 
sumptive evidence  of  such  a  pathology.  If  you  are  prepared  to 
accept  the  observations  which  I  have  put  before  you,  you  will 
agree  that  the  whole  question  of  asthma  has  to  be  revised. 
There  are  too  the  special  nocturnal  attacks  of  breathlessness  to 
which  elderly  patients  are  subject ;  we  require  special  observa- 
tions upon  these  cases  at  the  times  of  such  attacks. 

My  plea  is  not  that  you  will  accept  the  views  which  I  have 
put  forward  in  their  entirety,  but  that  you  should  recognise  how 
much  there  is  still  to  learn  on  the  question  of  dyspnoea ;  the  time 
has  come  when,  with  precise  methods  at  our  disposal,  we  must 
pause  until  such  knowledge  as  these  methods  may  produce  is 
acquired,  suspending  judgment  meanwhile,  but  frankly  ac- 


96  Chapter  IV 

knowledging  that  the  whole  pathology  of  constant  and  of  periodic 
dyspnoea  enters  upon  a  new  phase,  and  that  the  faiths  to  which 
we  have  adhered  in  the  past,  may  not  command  our  support  in 
the  future. 

At  our  feet  lie  pick  and  spade;  this  plot  of  land  cries  out  to 
us  to  take  them  up  and  bury  them  in  its  virgin  soil. 

EEFEBENCES 

Barcroft.     Eespiratory    Function   of   the   Blood.     London,    1914. 

(Full  references  to  other  papers  will  be  found  in  this  book.) 
Barcroft,  Peters,  Eoberts  and  Eyffel.     Journ.  of  PhysioL,  1913, 

XLV,  XLV. 
Beddard,     Pembrey    and     Spriggs.     Journ.     of    PhysioL,     1908, 

XXXVII,  XXXIX. 

Cook  and  Pembrey.     Journ.  of  PhysioL,  1908,  XXXVII,  LXVII. 
Geppert  and  Zuntz.     Archiv.  f.  d.  ges.  PhysioL,  1888,  XLIII,  189. 
Leymann.     Archiv.  f.  d.  ges.  PhysioL,  1888,  XLIII,  284. 
Lewis.     Brit.  med.  Journ.,  1913,  II,  Nov.  29th. 
Lewis,  Eyffel,  Woolf,  Cotton  and  Barcroft.     Heart,  1913,  V,  45. 
Poulton  and  Eyffel.     Journ.  of  PhysioL,  1913,  XLVI,  XLVII. 
Eyffel.     Journ.  of  PhysioL,  1909,  XXXIX,  XXIX. 
Straub  and  Schlayer.     Munch,  med.  Wochcnschr,  1912,  LIX,  569. 


AN  ADDRESS 

ENTITLED 

"OBSERVATIONS  UPON  CARDIAC 
SYNCOPE" 

DELIVERED  AT  THE  OPENING  OF  THE  FACULTY  OF  MEDICINE, 
McGiLL  UNIVERSITY,  MONTREAL,  OCTOBER  STH,  1914. 


CHAPTER  V 
OBSERVATIONS  UPON  CARDIAC  SYNCOPE 

Gentlemen, 

In  responding  to  the  invitation  which  you  have  done  me  the 
honour  of  sending  me,  I  have  chosen  "  Cardiac  Syncope  "  as  the 
subject  of  my  remarks  to-day. 

There  is  a  common  misconception  at  the  present  day  that  the 
study  of  the  heart's  action  by  modern  means  finishes  and  ends 
with  disorder  of  the  heart  beat;  that  indications  of  systole  of 
the  auricles  and  ventricles,  obtained  directly  or  indirectly  by 
mechanical  or  electrical  means,  are  simply  of  value  in  inter- 
preting and  classifying  irregularities  of  the  pulse  or  heart. 

The  electrocardiograph  and  the  polygraph,  recent  devices  for 
graphic  registration,  should  be  regarded  rather  as  individual 
means  to  a  specific  end,  research  upon  human  pathology  in  all 
its  phases  and  by  the  most  accurate  methods  which  may  be 
employed.  While  the  nature  of  disordered  heart  action  is  a 
study  rapidly  reaching  its  termination,  the  problems  which  such 
study  has  opened  up  are  manifold  and  far  reaching.  Our  gen- 
eral conceptions  of  heart  disease  are  rapidly  and  surely  altering, 
and  this  change  in  our  processes  of  thought  has  been  governed 
largely,  if  not  entirely,  by  the  widespread  adoption  of  the 
graphic  method.  The  method,  by  its  precision,  has  sharpened 
our  critical  faculties ;  it  has  insistently  emphasised  the  value  of 
close  observation  upon  the  actual  events  of  disease ;  in  short,  it 
has  created  in  this  field  of  work  an  atmosphere  of  refinement 
and  exactitude,  the  influence  of  which  at  present  dominates,  and 
will  in  the  future  dominate  the  world  of  cardiac  pathology.  It 
has  carried  this  branch  of  clinical  science  in  one  step  to  the  level 

99 


100  Chapter  V 

of  its  companion  sciences  of  the  laboratory;  it  has  awakened  a 
great  and  growing  dissatisfaction  with  traditional  cardiac  phil- 
osophy. Our  new  philosophy  is  deeply  rooted,  it  is  to  be  trained 
to  cover  a  hard  and  imperishable  wall  of  fact ;  the  old  philosophy 
entwines  a  neighbouring  trellis  whose  frailty  assumes  increasing 
prominence.  Graphic  experience  has  clearly  displayed  the  in- 
sufficiency and  the  weaknesses  of  the  older  methods ;  has  stressed 
the  need  of  searching  revision;  has  more  narrowly  denned  the 
bounds  of  legitimate  argument ;  has  condemned  those  nights  of 
imagination  which  have  been  responsible  in  the  past  for  pre- 
carious conceptions,  for  loose  reasoning;  has  reminded  us  in 
unmistakable  language  that  facts  are  our  only  sure  foothold,  the 
only  real  estate  which  we  bequeath  to  our  successors ;  has  warned 
us  once  again  to  realise  that  hypothesis  is  but  a  guide  to  observa- 
tion, and  that  dogma  has  no  place  in  the  pursuit  of  knowledge. 

My  purpose  in  the  present  address  is  to  take  one  of  many 
possible  illustrations  and  to  attempt  to  show  you  where  our  true 
knowledge  and  our  legitimate  conceptions  of  the  pathology  of 
cardiac  syncope  begin  and  end. 

It  is  advisable  that  I  define  for  you  at  the  outset  what 
I  intend  to  convey  in  the  present  address  by  the  term,  "  car- 
diac syncope  " ;  I  wish  to  convey  a  sudden  loss  of  conscious- 
ness which  is  due  to  a  derangement  of  the  heart's  function. 
We  may  pause  for  a  few  moments  to  consider  the  limits  of  this 
definition.  On  the  one  hand,  and  considered  strictly,  it  excludes 
such  symptoms  as  are  described  by  our  patients  as  "  f  aintness  " 
or  "  giddiness."  These  symptoms,  as  you  are  aware,  are  com- 
mon manifestations  of  heart  disease ;  not  infrequently  they  are 
produced  in  a  manner  similar  to  real  cardiac  syncope  as  I  have 
defined  it.  That  is  to  say  a  momentary  faintness  or  giddiness 
may  result  from  a  cause  of  identical  nature  with  that  which 
induces  loss  of  consciousness,  though  in  the  last  case  the  disturb- 
ance is  of  longer  duration.  To  some  extent,  therefore,  we  cannot 
refrain  from  alluding  to  these  symptoms ;  we  may  refrain  just 


Observations  Upon  Cardiac  Syncope  101 

in  so  far  as  may  be  necessary  to  maintain  the  discussion  within 
convenient  limits ;  thus  I  do  not  propose  to  consider  the  attacks 
of  faintness  or  giddiness  which  are  specially  associated  with 
aortic  disease.  On  the  other  hand,  our  definition  will  include 
many  forms  of  unexpected  death  in  cardiac  patients,  for  such 
death  as  we  shall  see  may  come  as  a  natural  sequence  of  events 
which  first  induce  simple  loss  of  consciousness. 

Again,  our  definition  will  exclude  all  possible  causes  of 
syncope  in  which  the  arterial  system  is  the  prime  malefactor. 
Cerebral  arterial  disease  is  a  subject  which  I  shall  not  consider. 
Neither  will  it  be  possible  more  than  to  refer  in  passing  to  one 
of  the  commonest  forms  of  syncope,  namely,  fainting  attacks  in 
young  people ;  I  mean  those  attacks  which  are  universally  and 
probably  rightly  attributed  to  vasomotor  disturbances  in  the 
splanchnic  area.  Briefly,  we  shall  concentrate  our  attention 
upon  the  heart  itself,  enquiring  especially  into  the  nature  of 
attacks  of  unconsciousness  which  are  unquestionably  associated 
with  disordered  rhythm  or  into  the  nature  of  unexpected  death 
supposedly  of  similar  origin. 

Causes  of  cardiac  syncope  and  unexpected  deaths 
of  cardiac  origin. 

Amongst  the  causes  of  sudden  and  unexpected  death  of  cardiac 
origin  there  are  several  which  have  been  completely  understood 
for  a  long  while.  Embolic  plugging  of  the  pulmonary  artery 
and  impaction  of  a  ball  thrombus  in  a  narrowed  mitral  orifice 
are  recognised  causes  of  such  death;  in  each  instance  the  chief 
channel  is  abruptly  and  completely  obstructed  and  the  circula- 
tion is  brought  to  an  immediate  standstill.  In  hospital  patients, 
in  whom  there  has  been  a  sudden  catastrophe,  a  third  cause  is 
always  sought  at  autopsy,  namely,  plugging  of  a  main  coronary 
artery  or  a  chief  branch.  Upon  this  accident  I  shall  have  more 
k  to  say  presently.  Another  terminal  event  is  rupture  of  the 
heart  wall,  or  rupture  of  an  aortic  aneurism  into  the  pericardium 


102  Chapter  V 

or  pulmonary  artery.  These  causes  of  unexpected  death  are, 
for  the  most  part  mechanical,  and  on  that  account  have  appealed 
forcibly  to  pathologists  in  the  past;  for  they  are  capable  of 
demonstration  in  the  post-mortem  room.  But  how  often  does 
the  examination  proceed  to  its  termination  upon  the  bodies  of 
patients  who  have  collapsed  unexpectedly,  without  the  discovery 
of  the  cause  of  death?  In  the  majority  of  patients  who  have 
died  of  cardiac  syncope  in  the  past,  no  lesion  has  been  found 
which  could  be  said  to  be  directly  responsible.  It  is  precisely 
this  type  of  syncope  to  which  I  propose  to  devote  chief  atten- 
tion; and  for  several  reasons.  In  the  first  place,  because  it 
begins  to  be  more  fully  understood ;  in  the  second  place,  because 
by  its  study  we  may  be  forewarned  of  its  approach  in  given  cases 
and  may  adopt  suitable  measures  for  its  prevention.  You  will 
find  a  good  deal  has  been  said,  but  that  little  or  nothing  has 
been  known  concerning  sudden  diastolic  arrest  of  the  heart,  or, 
as  the  French  physicians  term  it,  asystole.  These  terms  mean 
no  more  than  that  the  heart  ceases  to  beat. 

You  will  read  of  spasm  or  cramp  of  the  muscle,  conditions 
unknown  to  physiology;  equally  unknown  to  pathology.  You 
will  all  have  heard  accounts  of  patients  who  succumb  to  a 
mysterious  malady,  angina  sine  dolore.  Such  terms  bring  us 
no  nearer  the  truth ;  give  us  no  clearer  conception  of  the  cause  of 
death. 

The  causes  of  unexpected  death  are  to  be  discovered  by 
laboratory  experiment,  and  especially  by  observations  upon 
recurrent  cardiac  syncope  in  the  human  being.  It  is  to  the  last 
source  that  we  owe  most  of  our  knowledge  to-day.  What  then  do 
we  know  positively  of  cardiac  syncope  ?  We  know  that  it  may 
be  produced  in  a  variety  of  ways,  which  may  be  classed  under 
two  broad  headlines,  (1)  retardation  or  cessation  of  the  ventricu- 
lar action;  (2)  acceleration  of  the  ventricular  beating.  Under 
the  first  heading  we  may  consider  (a)  slowing  or  standstill  of 
the  whole  heart  (&)  slowing  or  standstill  of  the  ventricle. 


Observations  Upon  Cardiac  Syncope  103 

Under  the  same  heading  we  may  discuss  (c)  ventricular  fibril- 
lation. 

Slowing  or  standstill  of  the  whole  heart. 
There  are  now  a  number  of  cases  upon  record  in  which  attacks 
of  cardiac  syncope  may  be  definitely  ascribed  to  standstill  of 
the  whole  heart.  The  most  perfect  example  of  its  kind  was 
described  by  Laslett  a  few  years  ago.  The  syncopal  attacks 
were  associated  with  intermissions  of  the  heart  action  of  4-8 
seconds  duration.  An  example  of  the  curves,  which  demon- 
strate cessation  of  both  auricular  and  ventricular  action,  is  seen 
in  Fig.  72,  which  is  from  this  case.  The  attacks  were  fre- 


Jugular 


Fig.  72.     Venous  and  radial  curves  during  a  syncopal  attack,  due  to  va- 
gal  standstill  of  the  whole  heart.      (After  Laslett.) 

quently  repeated,  sometimes  at  intervals  of  a  few  moments ;  al- 
most certainly  they  were  produced  through  the  medium  of  the 
vagus,  for  atropine  abolished  them. 

A  case  which  probably  belongs  to  the  same  category  has  been 
recorded  by  Neubiirger  and  Edinger.  Frequent  syncopal 
attacks,  in  which  the  pulse  failed,  were  observed  in  a  man  who, 
at  autopsy,  exhibited  a  small  aneurism  upon  the  basilar  artery; 
the  attacks  came  with  effort,  or  at  such  times  as  a  rise  of  blood 
pressure  might  be  held  to  account  for  enlargement  of  the  tumour 
with  pressure  on  the  vagal  centre  in  the  medulla.  This  patient 
succumbed  to  a  seizure  of  the  kind.  Their  report  is  most  sug- 
gestive and  striking,  and  it  is  only  to  be  regretted  that  at  the 
time  graphic  methods  had  not  sufficiently  developed. 

Syncope  which  is  the  result  of  standstill  of  the  whole  heart 
is  a  rare  phenomenon. 


104  Chapter  V 

Standstill  of  the  ventricle. 

A  more  frequent  cause  of  cardiac  syncope  is  standstill  of  the 
ventricle,  the  auricle  continuing  to  beat  at  about  its  former  rate ; 
this  event  is  associated  with  heart-block.  It  is  convenient  in 
dealing  with  this  subject  to  sub-group  the  clinical  cases. 

Sudden  development  of  heart-block.  Syncope  may  come 
without  warning  in  patients  who  present  a  perfectly  normal 
heart  mechanism  up  to  the  time  of  the  attack.  For  illustration 
of  this  form  of  seizure  I  may  cite  a  case  which  recently  came 
under  my  care.  A  man  of  48  years,  suffering  from  chronic 
aortic  stenosis,  had  for  some  years  experienced  attacks  of  gid- 
diness followed  often  by  a  temporary  lapse  of  consciousness ;  they 
came  without  warning,  and  sometimes  he  fell  heavily.  When 
seen,  the  attacks  were  of  irregular  frequence,  but  numerous, 
ranging  in  number  from  one  or  two  to  several  hundred  in  the 
day.  On  several  occasions  I  talked  to  him  while  he  sat  in  a 
chair,  and  from  time  to  time,  as  he  replied  to  my  questions,  a 
sudden  and  intense  pallor  overspread  his  features;  he  be- 
came abruptly  silent,  the  pupils  dilated,  respiration  deepened 
and  a  little  squint  and  general  rigidity  developed ;  consciousness 
might  or  might  not  be  lost  momentarily.  In  a  little,  the 
face  became  intensely  flushed,  he  moved  and  gradually  regained 
complete  mental  control.  An  example  of  the  curves,  showing 
the  events  accompanying  two  attacks,  is  given  in  Fig.  Y3. 

The  mechanism  of  the  heart,  before  and  after  the  attack 
was  perfectly  natural;  during  the  attack  the  pulse  failed  for 
a  period  of  3  to  8  seconds;  a  lapse  of  5  seconds  was  sufficient 
to  abolish  consciousness.  During  the  period  of  standstill,  the 
heart  sounds  were  in  abeyance,  but  the  auricles  continued  to 
beat  at  their  former  rate.  The  offset  was  accompanied  by 
accelerated  heart  action  and  a  rapid  rise  of  blood  pressure. 
In  this  patient  atropine  failed  to  give  relief.  In  the  absence 
of  a  cellular  examination  of  the  heart,  the  cause  of  the  heart- 


Observations  Upon  Cardiac  Syncope  105 


£)     O 

-1 

-~   &* 


01  v. 

^5  ~ 


106  Chapter  V 

block  cannot  be  denned  accurately,  but  as  the  patient  has  more 
recently  developed  complete  dissociation  of  the  auricles  and 
ventricles,  it  seems  probable  that  a  lesion  of  the  A-V  bundle  was 
responsible  for  them.  Some  years  ago  I  saw  a  somewhat  similar 
case;  in  this  instance  fits  came  in  groups  between  intervals  of 
freedom  which  lasted  several  months;  on  the  days  when  they 
were  experienced,  partial  heart-block  of  low  grade  was  found. 
This  patient  died  as  a  result  of  a  fall  during  an  attack  and  Dr. 
Cohn  examined  the  heart  for  me.  He  found  large  blood  sinuses 
in  the  A-V  bundle,  the  tissue  having  almost  the  appearance  of 
a  nsevus ;  it  is  easy  to  comprehend  how  in  this  instance  an  added 
strain  with  engorgement  of  those  vessels  would  bring  about  cessa- 
tion of  the  ventricular  beating. 

Increase  of  pre-existing  block.  Syncope  is  a  very  frequent 
accident  in  patients  who  are  the  subjects  of  chronic  partial  heart- 
block,  where  for  example  the  auricles  beat  at  exactly  twice  the 
rate  of  the  ventricles;  in  all  such  cases  it  is  due  to  a  sudden 
increase  in  the  degree  of  block,  the  ventricle,  which  originally 
responded  to  alternate  auricular  impulses,  remaining  inert  for  a 
variable  period. 

Two  explanations  of  the  sudden  exaggeration  of  the  conduc- 
tion defect  in  these  patients  have  been  put  forward.  In  some 
instances,  for  example  in  the  case  reported  by  Erlanger,  the 
ventricular  silence  was  preceded  by  a  period  of  auricular  quick- 
ening. Now  when  partial  heart-block  is  present,  its  degree  is 
enhanced  by  acceleration  of  the  auricles,  and  the  net  result  is 
a  fall  of  ventricular  rate  which  may  amount  to  a  standstill.  It 
may  be,  therefore,  that  the  fits  of  partial  heart-block  are  pro- 
duced in  this  manner  in  some  patients.  It  has  also  been  sup- 
posed that  the  exaggerated  block  is  produced  by  vagal  influ- 
ences; undoubtedly  the  vagus  is  capable  of  producing  this 
increase  of  block,  as  has  been  shown  by  Rihl  and  others  who 
have  occasioned  fits  in  these  patients  by  pressing  upon  the  vagus 
in  the  neck;  but  the  effects  of  atropine  are  uncertain  and  too 


Observations  Upon  Cardiac  Syncope  107 

often  negative.     The  actual  provocative  cause  in  most  cases  is 
still  unknown. 

Ventricular  standstill  in  complete  heart-block.  The  highest 
grade  of  heart-block  is  that  in  which  auricle  and  ventricle  are 
dissociated,  each  beating  regularly  and  at  its  own  inherent  rate. 
In  such  patients,  the  auricular  rate  is  70  per  minute  or  a  little 
higher ;  the  ventricular  rhythm  has  a  usual  rate  of  30  to  40  per 
minute ;  this  rhythm  is  developed  in  the  ventricle  itself,  and  in 
all  probability  in  the  auriculo-ventricular  bundle.  These  pa- 
tients are  by  no  means  exempt  from  syncopal  attacks ;  the  major- 
ity suffer  from  them.  Here  too,  the  fits  are  the  result  of  ventric- 
ular stoppage  (Fig  74).  Erlanger  and  Blackman  have  suc- 
ceeded in  reviving  dogs  after  crushing  the  A-V  bundle,  and  in 
several  of  these  animals  characteristic  syncopal  attacks  devel- 
oped. Now  although  the  vagus  has  an  undoubted  influence  upon 
the  mammalian  ventricle,  it  is  improbable  that  this  nerve  can  be 
held  responsible  for  the  additional  ventricular  slowing ;  for  fits 
could  not  be  produced  by  stimulation  of  the  vagus  in  Erlanger's 
experiments ;  and  there  is  a  growing  consensus  of  opinion  that 
the  influence  of  the  vagus  upon  the  ventricle,  dissociated  from 
the  auricles  by  lesion,  is  slight ;  it  seems  probable  that  most  of 
the  vagal  fibres  run  to  the  ventricle  along  the  same  tract  as  the 
auriculo-ventricular  muscle  fibres.  Attention  directs  itself 
therefore  to  the  centre  which  forms  the  independent  ventricular 
rhythm,  and  especially  to  its  nutrition.  The  centre  is  localised 
in  the  main  stem  of  the  bundle  immediately  below  the  lesion 
which  produces  the  original  heart-block.  This  tissue  is  often 
diseased  in  the  patients  whom  we  are  considering;  that  is  to 
say  the  tissue  upon  which  the  ventricle  depends  for  its  rhythm 
is  presumed  to  be  in  an  abnormal  state;  little  wonder,  in  such 
circumstances,  if  rhythm  production  in  this  region  is  from  time 
to  time  impaired.  A  single  case  has  been  recorded  in  which  the 
fits  of  complete  heart-block  received  complete  explanation.  The 
independent  ventricular  rhythm  is  influenced  in  a  notable 


108 


Chapter  V 


fashion  by  stimulation  of  the  ventricle.  Originally  slow,  its 
rate  may  be  artificially  enhanced  by  interrupted  stimulation, 
and  a  higher  rate  of  beating  may  be  maintained  in  this 
fashion  over  indefinite  periods ;  but  if  at  any  time  stimulation 
ceases,  the  independent  rhythm  shows  unwillingness  to  return; 
it  takes  time  to  develop  and  prolonged  standstill  results.  In  a 
patient  who  was  the  subject  of  complete  heart  block,  the  ventric- 
ular rate  was  constantly  30  per  minute,  but  from  time  to  time 
a  new  rhythm  of  extra-systolic  nature  developed,  driving  the 
ventricle  at  YO  or  more  per  minute.  At  the  cessation  of  this 
rhythm,  standstill  of  the  ventricle,  associated  with  syncope  (and 
in  the  last  attacks  with  syncope  terminating  in  death)  was  the 
rule. 

A  chart  of  the  ventricular  beats  in  this  patient,  constructed 
from  curves  taken  over  a  long  period,  is  shown  in  Fig.  75. 


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Fig.  75.  A  diagram  compiled  from  a  continuous  curve  of  the  apex  beat, 
the  duration  of  which  was  21  minutes.  The  diagram  reads  from  left 
to  right,  following  consecutive  lines.  Each  beat  of  the  original  curve 
has  been  charted  on  a  large  scale  and  the  chart  has  been  reduced  sub- 
sequently photographically.  The  vertical  lines  are  placed  at  two- 
second  intervals.  The  relation  of  the  (relative)  tachycardial  periods 
to  the  long  asystolic  intervals  is  very  clearly  shown. 


Observations  Upon  Cardiac  Syncope  109 

The  relation  of  standstill  to  the  preceding  acceleration  of 
ventricular  rate  is  clearly  shown  in  this  diagram. 

Cerebral  ancemia  and  its  effects.  In  the  forms  of  cardiac 
syncope  which  we  have  considered  the  output  from  the  left 
ventricle  is  diminished  and  arterial  blood  pressure  falls  almost 
to  zero;  the  subjective  manifestations  are  the  result  of  cerebral 
anaemia.  The  events  which  follow  defective  blood  supply  to  the 
brain,  are  well  known;  severe  haemorrhage  is  quickly  followed 
by  loss  of  consciousness ;  in  the  slaughtering  of  sheep  the  carotids 
are  severed,  the  animals  fall  unconscious  almost  immediately 
and  after  a  little  while  convulsive  movements  are  exhibited. 
Kussmaul  and  Tenner  compressed  the  carotid  arteries  in  a  num- 
ber of  male  adults ;  pallor  of  the  face  followed  and  the  pupils 
dilated ;  "  as  soon  as  the  dilatation  of  the  pupils  began  to  take 
place,  the  respirations  became  slow,  deep,  and  as  it  were  sighing. 
Afterwards  dizziness,  staggering  and  unconsciousness  ensued." 
In  two  instances  vomiting  and  convulsions  were  noted  as  com- 
pression was  continued.  Schiff  and  Hill  have  produced  uni- 
lateral convulsions  by  the  compression  of  one  carotid. 

You  are  aware  that  consciousness  is  often  lost  in  hutch  rabbits 
if  they  are  held  a  short  while  by  the  ears  and  that  this  is  due  to 
an  effect  of  gravity,  namely  to  accumulation  of  blood  in  the 
abdomen.  In  a  number  of  patients,  when  the  abdominal  walls 
are  lax,  momentary  giddiness  may  be  caused  by  sudden  assump- 
tion of  the  erect  posture ;  in  those  who  complain  of  this  symptom, 
rising  to  the  erect  posture  is  associated  with  a  demonstrable  and 
considerable  fall  of  blood  pressure. 

It  was  Webster  who  first  showed  that  in  Adams-Stokes 
syndrome  the  fit  is  preceded  by  pulse  slowing ;  and  since  his  time 
the  events  of  the  fit  have  been  carefully  studied,  especially  in 
cases  of  heart-block.  Cessation  of  the  ventricular  contraction 
comes  first,  and  is  speedily  succeeded  by  general  pallor  of  the 
skin;  dilatation  of  the  pupils,  giddiness  and  dimness  of  vision 
quickly  follow ;  if  the  ventricular  silence  is  continued,  conscious- 


110  Chapter  V 

ness  is  lost  and  epileptic  phenomena  consisting  chiefly  of  twitch- 
ings  of  the  facial  muscles,  movements  of  the  eye-balls  and  jerk- 
ing of  the  upper  limbs  are  added.  In  a  few  cases  the  convulsion 
becomes  general,  but  the  movements  are  rarely  violent.  The 
objective  signs  of  venous  stains  complicate  the  picture  when  the 
fit  lasts.  Termination  in  death  is  not  infrequent.  The  charac- 
ter of  the  attack  is  controlled  in  the  main  by  its  duration, 
recovery  may  come  at  any  stage,  and  is  preceded  by  a  return 
of  the  pulse  beats.  The  nervous  phenomena  witnessed  in  these 
syncopal  attacks  are  entirely  accounted  for  by  cerebral  anaemia 
resulting  from  cessation  of  the  circulation.  If  we  study  the 
accounts  which  have  been  published,  we  shall  find  that  although 
there  are  notable  individual  idiosyncrasies,  standstill  of  the 
ventricle  for  a  period  of  3-5  seconds  usually  produces  uncon- 
sciousness; at  the  end  of  15-20  seconds  epilepsy  commences;  an 
absence  of  ventricular  contraction  for  90-120  seconds  is  rarely 
followed  by  recovery. 

Although  abrupt  cessation  of  the  ventricular  beating  is  the 
rule  in  these  forms  of  syncope,  simple  slowing  may  be  responsible 
for  it.  A  fall  of  heart  rate  to  a  range  of  from  8-15  beats  per 
minute  is  rarely  tolerated  without  the  patient  passing  into 
a  condition  of  coma. 

Fibrillation  of  the  ventricles. 

It  is  a  remarkable  fact  that  practically  every  form  of  ir- 
regularity, which  has  been  produced  experimentally  in  the 
mammalian  heart,  has  now  been  recorded  frequently  in  clinical 
cases.  But  there  is  one  notable  exception.  We  know  that  the 
rhythmic  contraction  of  the  human  auricle  is  often  disturbed  by 
extrasystoles,  paroxysms  of  rapid  action  and  fibrillation;  we 
know  that  the  experimental  ventricle  is  subject  to  parallel  disor- 
ders, and  that  extrasystoles  and  rapid  action  may  originate  in  the 
human  ventricle ;  but  with  one  or  two  rare  instances,  fibrillation 
of  this  chamber  has  not  been  witnessed  clinically.  Fibrillation 


Observations  Upon  Cardiac  Syncope  111 

of  the  human  auricles  has  heen  proved  beyond  doubt  to  be  the 
most  frequent  cause  of  disordered  heart  action ;  why  is  fibrilla- 
tion of  the  ventricle  so  uncommon  an  experience  ?  For  a  good 
reason:  Fibrillation  of  the  ventricles  is  incompatible  with  ex- 
istence. When  the  ventricles  fibrillate,  the  co-ordinate  beat  of 
these  chambers  is  lost ;  the  muscle  is  divided  up  into  small  areas, 
which  show  independent  activities ;  as  a  result  the  output  of  the 
heart  ceases  abruptly,  the  blood  pressure  falls  to  zero,  the  circu- 
lation is  at  a  standstill.  In  other  words,  fibrillation  of  the  ven- 
tricle, if  it  occurs  in  man,  is  responsible  for  unexpected  and 
sudden  death.* 

We  have  the  strongest  a  priori  grounds  for  the  belief  that  sud- 
den death  comes  in  this  way  in  many  patients,  f 

Unexpected  death  in  cases  of  fibrillation  of  the  auricle. 

Sudden  and  unexpected  death,  attributable  to  this  cause,  is 
most  common  amongst  heart  patients  who  present  fibrillation 
of  the  auricles.  It  is  a  not  infrequent  termination  in  these 
patients;  the  conditions  necessary  to  persistent  fibrillation  of 
the  auricles  are  present  and  it  is  largely  for  this  reason  that  the 
form  of  death  which  I  shall  describe  to  you  is  attributed  to 
fibrillation  of  the  ventricles.  These  patients  are  often  admitted 
to  hospital  suffering  from  all  the  classical  signs  of  cardiac 
failure;  they  are  treated  with  digitalis,  often  in  considerable 
doses,  and  react  admirably  to  this  drug,  for  the  ventricular  rate 
slows,  while  breathlessness,  cyanosis,  venous  and  liver  engorge- 
ment and  dropsy  subside  or  vanish.  From  time  to  time  a 
sudden  and  unexpected  catastrophe  happens;  regarded  as  con- 

*  In  some  animals,  fibrillation  may  be  a  temporary  event;  but  this  is 
rare  and  is  seen  chiefly  in  the  rat,  rabbit  and  cat.  In  the  dog,  fibrillation 
is  nearly  always  terminal. 

t  The  suggestion  that  fibrillation  of  the  ventricles  may  be  responsible  for 
sudden  death  was  first  made  by  MacWilliam;  I  made  the  same  suggestion 
five  years  ago  in  writing  on  auricular  fibrillation.  Hering  and  others  have 
since  adopted  the  same  view. 


112 


Chapter  V 


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valescent  the  patient  is  sitting  in  bed, 
chatting  or  feeding  may  be.  A  nurse 
in  charge  or  perhaps  a  neighbouring 
patient  hears  a  cry  or  choking  sound; 
the  patient  falls  back  on  the  pillows  in- 
tensely pale,  there  are  a  few  gasping 
respirations,  a  little  convulsive  move- 
ment, and  the  pulseless  patient,  rapidly 
becoming  livid,  is  still.  These  are  the 
symptoms  which  follow  when  fibrilla- 
tion develops  in  an  experimental  ani- 
mal; it  is  hardly  to  be  doubted,  consid- 
ering the  circumstances,  that  the  same 
event  terminates  the  life  of  the  patient. 

The  fatal  accident  may  happen  in  the 
untreated  disease,  or  it  may  happen 
when  any  drug  of  the  digitalis  group 
(strophanthine,  etc.)  is  given  in  excess; 
the  same  drugs  given  in  poisonous  doses 
to  animals  will  induce  ventricular  fibril- 
lation. In  the  administration  of  digi- 
talis in  cases  of  auricular  fibrillation 
the  period  of  danger  is  marked  by  the 
appearance  of  a  bigeminal  pulse  (Fig. 
76)  ;  upon  analysis  this  bigeminy  is 
found  to  result  from  extrasystoles  of 
ventricular  origin,  beats  which  are  fre- 
quent precursors  of  fibrillation  in  ex- 
periment. 

A  few  isolated  instances  of  curves 
purporting  to  show  fibrillation  of  the 
ventricles  in  the  human  subject  have 
been  published.  In  one  of  several 
curves  recorded  bv  Robinson  and 


Observations  Upon  Cardiac  Syncope  113 

Draper  from  moribund  or  dead  patients,  fibrillation  is  de- 
picted. Hoffman  has  recorded  an  instance  of  syncope  in  which 
the  electrocardiograms  are  interpreted  in  the  same  fashion,  but 
the  analyses  of  these  curves  are  open  to  question.  The  actual 
events  in  unexpected  death  are  still  in  a  measure  uncertain; 
nevertheless  the  assumption  of  ventricular  fibrillation  is 
strongly  supported.* 

Death  from  chloroform.     Recently  some  remarkable  observa- 


Fig.  77.  Three  electrocardiograms  from  a  cat  anaesthetised  with  a  weak 
chloroform  vapour.  After  a  minute  dose  of  adrenalin  extrasystoles  of 
ventricular  origin  appeared  (a).  These  became  more  frequent  until  the 
heart  responded  entirely  to  new  impulses  of  ventricular  origin  (6). 
In  a  short  while  fibrillation  commenced  (c). 

tions  have  been  made  by  Levy.  He  has  shown  in  a  very  conclu- 
sive manner  that  death  during  the  administration  of  chloroform 
to  cats  is  almost  always  due  to  the  onset  of  this  curious  derange- 
ment of  the  heart  beat  and  that  it  comes  when  the  heart  is 
rendered  suspectible  by  small  percentages  of  the  vapour  (Fig. 
77).  Levy  goes  further  and  makes  out  an  extremely  strong  case 
for  his  view  that  the  majority  of  chloroform  fatalities  in  the 

*  Dr.  Halsey  of  New  York  has  recently  shown  me  a  convincing  example 
of  death  from  fibrillation. 


114 


Chapter  V 


>»  -J  £   b 


5  * 


* 


human  subject  are  due 
to  ventricular  fibrilla- 
tion. As  he  points  out 
and  emphasises,  most  of 
these  fatalities  occur  in 
the  induction  stages  or 
at  other  periods  of  the 
administration  w  hen 
the  saturation  of  the 
blood  with  chloroform 
is  relatively  low.  The 
susceptibility  of  the 
cat's  heart  has  recently 
been  confirmed  by  Mac- 
William  ;  Levy  has 
studied  the  question  in 
such  detail  that,  prac- 
tically speaking,  he  can 
produce  the  condition 
and  its  associated  syn- 
cope at  will.  His  work 
upon  this  subject  is  a 
landmark  in  the  history 
of  research  upon  death 
under  chloroform. 

Death  in  other  condi- 
tions. Fibrillation  of 
the  ventricles  is  almost 
certainly  the  terminal 
event  in  many  cases  of 
death  from  lightning 
(Jex-Blake).  Patho- 
logical observation  also 
teaches  that  it  is  in 


Observations  Upon  Cardiac  Syncope  115 

this  manner  that  the  circulation  fails  in  embolism  of  a 
coronary  artery.  These  experiments  date  from  Cohnheim's 
researches.  When  a  coronary  artery,  or  often  when  a  small 
branch  of  such  a  vessel  is  obstructed  in  an  animal,  there  follows 
within  a  short  space  of  time  a  series  of  remarkable  disorders  of 
the  heart  beat.  First  the  regular  rhythm  is  disturbed  by  a 
ventricular  extrasystole,  then  by  short  runs  of  these  beats  occur- 
ring successively;  a  little  later  they  may  be  so  arranged  as  to 
constitute  short  or  long  paroxysms  of  tachycardia  (Fig.  78)  ;  the 
final  event  is  fibrillation  of  the  ventricle  and  when  this  comes  the 
animal  dies.  It  is  precisely  the  same  train  of  events  as  is  seen 
in  chloroform  poisoning;  a  gradual  succession  of  ventricular 
disorders  of  ever  increasing  complexity.  The  relation  of  oblit- 
eration of  a  coronary  vessel  to  fibrillation  of  the  ventricles  never- 
theless is  not  completely  understood.  It  is  probable  that  it  fol- 
lows acute  obstruction  only,  for  it  is  not  a  rare  thing  to  find  the 
coronary  artery  almost  or  completely  occluded  by  a  long  standing 
lesion  in  human  hearts.  The  coronary  vessels  are  not  end-arter- 
ies, the  anastomoses  are  clearly  displayed  by  Spalteholz's  method 
and  blood  is  often  to  be  found  beyond  a  complete  and  old  ob- 
struction. If  you  watch  the  muscle  supplied  by  a  coronary 
branch  upon  which  a  ligature  is  placed,  you  will  notice  that  it 
first  becomes  livid  and,  as  it  loses  its  function,  it  balloons  with 
each  heart  beat ;  it  is  at  this  stage  that  irregularity  of  the  heart 
is  noticed,  if  it  occurs  at  all;  but  often  the  livid  area  revives 
as  the  anastomosing  vessels  open  up  and  the  disorder  of  the 
heart  beat  vanishes.  Obstruction  to  a  small  branch  may  or  may 
not  prove  fatal  in  the  animal ;  that  it  may  not  prove  fatal  in  man 
is  evidenced  by  the  appearance  of  fibrotic  patches  in  the  muscu- 
lar wall  which  may  be  attributed  to  arterial  occlusion ;  obstruc- 
tion of  a  main  coronary  in  an  animal  is  not  necessarily  fatal 
during  the  period  of  an  experiment,  though  recovery  is  rarely 
seen.  I  would  especially  emphasise  the  possibility  that  certain 
of  the  cases  of  sudden  death  in  heart  disease  are  due  to  plug- 


116 


Chapter  V 


ging  of  vessels  supplying  relatively  small  or  deeply  seated  areas 
of  muscle;  such  vessels  are  not  often  examined  at  autopsy. 

Accelerated  heart  action. 

The  last  cause  of  syncope  which  I  propose  to  consider  is 
acceleration  of  the  heart's  action.  The  normal  mammalian 
heart  has  a  wonderful  reserve  power  and  capacity  of  accommoda- 
tion. You  may  artificially  increase  its  rate  by  stimulating  it 
with  serial  induction  shocks  over  a  wide  range  of  rate,  without 
materially  influencing  the  peripheral  circulation.  The  effect  of 
acceleration  in  the  circumstances  is  to  curtail  diastole;  as  a 
consequence  diastplic  pressure  rises  and  systolic  pressure  falls ; 
the  mean  pressure  is  maintained.  But  even  in  the  normal  heart 


Fig.   79.     Electrocardiograms   from    leads   /   and   II   showing   an   auricular 
and  a  ventricular  rate  of  270  in  a  child.     Auricular  flutter. 

there  is  a  limit  of  this  accommodation  and,  as  the  rate  rises,  a 
time  comes  when  the  diastolic  periods  are  so  curtailed  that  filling 
is  incomplete.  The  mean  pressure  then  falls.  If  the  heart  is 
abnormal  or  its  efficiency  is  damaged,  the  effects  of  acceleration 
are  more  speedily  felt;  a  rise  of  rate,  which  would  create  no 
material  disturbance  under  ordinary  conditions,  in  these  circum- 
stances would  have  profound  effects.  Some  curious  examples 
and  contrasts  have  come  to  my  notice.  I  recall  an  instance  in 
which  a  regular  acceleration  of  the  heart's  action  to  160  and 


Observations  Upon  Cardiac  Syncope  117 

more  per  minute  had  been  present  for  several  years ;  the  patient 
was  under  my  observation  for  several  months,  and  this  rate  was 
constant;  yet  the  disturbance  was  comparatively  slight,  consist- 
ing only  of  a  sense  of  exhaustion  with  and  after  effort. 

Recently  a  child  was  brought  to  me  for  examination  in  which 
the  ventricular  rate  remained  at  270-290  during  several  hours  of 
observation  (Fig.  79)  ;  the  curves  from  this  child  were  taken 
while  it  slept  or  while,  in  a  waking  state,  it  peacefully  took  its 
food.  But  such  rates  are  very  exceptional,  and  are  tolerated 
only  by  sound  muscle.  Where  there  is  muscle  damage  a  rate  of 
160-200  is  rarely  tolerated,  and  higher  rates  speedily  induce 
signs  of  grave  circulatory  embarrassment.  This  embarrass- 
ment comes  in  the  way  I  have  indicated ;  by  a  reduction  of  di- 
astole, arterial  pressure  is  lowered  and  venous  pressure  is  raised 
(Fisr.  80). 


_         #»  #T 

•i*T '..fUr  ^ 


80.  Hiirthle  curve  of  arterial  pressure  and  electrocardiogram.  Show- 
ing the  fall  of  arterial  pressure  which  occurs  when  the  heart's  action 
is  greatly  accelerated  by  stimulation. 

Simple  paroxysms  of  regular  tachycardia  are  prone  to  pro- 
duce actual  attacks  of  syncope  in  susceptible  subjects ;  giddiness 
during  the  seizures  is  a  common  manifestation  (Fig.  81). 
These  symptoms  are  often  to  be  ascribed  to  lessened  cardiac  out- 
put and  the  consequent  fall  of  arterial  pressure. 

I  show  you  an  example  in  Fig.  82  where  two  short  paroxysms 
of  regular  tachycardia  (rate  200-220  per  minute)  are  recorded; 
these  were  accompanied  by  giddiness,  others  of  longer  duration 
by  severe  giddiness  verging  on  loss  of  consciousness;  at  times 
the  same  patient  actually  fainted.  You  will  notice  the  lowering 


118 


Chapter  V 


J^g  'S 


j 


&  I 


/  02 

I     I 


Observations  Upon  Cardiac  Syncope 


119 


of  the  pulse  line,  indicating  reduction  of  the  blood  pressure,  as 
•each  paroxysm  proceeds.  Several  cases  are  upon  record  in 
which  Adams-Stokes  syndrome  was  simulated  by  paroxysms  of 
this  kind,  for  the  beats  of  the  paroxysm  failed  to  force  a  suf- 
ficiency of  blood  into  the  arteries  and  consciousness  during  the 
attacks  was  frequently  lost. 

Another  condition  in  which  giddiness  or  actual  syncope  is  seen 
is  paroxysmal  auricular  fibrillation,  and  the  cause  is  the  same  in 
this  malady.  For  the  fibrillation  in  the  auricles  drives  the 
ventricles  at  a  greatly  accelerated  rate  during  the  attack,  and  as 
a  result,  mean  arterial  pressure  may  be  considerably  reduced. 


-4—1: 

Fig.  83.  Electrocardiograms  from  lead  II  and  ///,  showing  auricular  flut- 
ter. The  ventricular  rate  is  165,  the  auricular  rate  330.  This  pa- 
tient suffered  from  syncopal  attacks  which  were  proved  to  result  from 
the  assumption  of  the  full  auricular  rate  by  the  ventricle. 

There  is  a  disorder  of  considerable  clinical  importance  which 
has  but  recently  been  discovered.  It  is  a  condition  found  in 
adults  for  the  most  part,  in  which  the  auricles  beat  at  extreme 
rates,  reaching  and  surpassing  320  per  minute.  It  may  be  taken 
as  a  general  rule  that  in  this  state,  which  has  been  termed  auric- 
ular flutter,  the  ventricle  does  not  respond  to  the  full  auricular 
rate;  it  responds  to  alternate  auricular  impulses  (Fig.  83),  and 
its  rate  is  thus  halved.  If  the  auricles  beat  at  320,  the  ventricu- 
lar rate  is  160;  the  ventricular  rate  of  160  is  usually  sufficient 


120  Chapter  V 

materially  to  embarrass  the  circulation  in  these  people;  how 
much  greater  the  strain  when  the  full  rate  is  experienced  ?  I 
question  whether  any  adult  heart,  normal  or  abnormal,  could 
long  maintain  this  rate  of  beating;  certain  it  is  that  with  this 
heart  rate,  the  cerebral  circulation  would  be  grossly  insufficient. 
Now  patients  who  are  sufferers  from  auricular  flutter  and  in 
whom  there  is,  so  to  speak,  a  potential  ventricular  rate  of  300  or 
more  per  minute,  frequently  experience  syncopal  attacks  and  it 
has  recently  been  shown  by  the  graphic  method  that  such  attacks 
are  the  result  of  the  temporary  development  of  the  full  ven- 
tricular rate.  It  should  be  remembered  that  the  auricle  is  send- 
ing forth  impulses  at  300  per  minute  and  that  the  ventricle 
usually  refuses  half  these  demands  to  contract ;  now  and  again 
the  full  call  is  answered,  the  heart  rate  leaps  to  its  fullest,  arterial 
blood  pressure  sinks  rapidly,  the  brain  is  insufficiently  sup- 
plied, unconsciousness  supervenes  and  is  maintained  while  the 
ventricle  gallops  uncurbed. 

In  the  light  of  these  observations,  the  syncopal  attacks  of 
paroxysmal  tachycardia  receive  adequate  explanation;  death 
during  such  attacks  —  unexpected  death  in  these  subjects  is  not 
very  infrequent  —  is  to  be  explained  by  a  prolongation  of  the 
seizures  or,  in  certain  instances,  may  be,  to  the  intervention  of 
another  disorder  which  we  have  already  considered,  namely, 
fibrillation  of  the  ventricles. 

Gentlemen,  the  facts  which  I  have  now  related  to  you  con- 
stitute our  chief  knowledge  of  the  causes  of  cardiac  syncope 
and  unexpected  death  in  heart  patients.  There  are  still  evident 
gaps  to  fill;  gaps  which  will  be  filled  in  the  near  future.  My 
purpose  has  been  not  only  to  record  our  present  knowledge  in 
this  single  direction  but  to  point  to  the  trend  of  modern  ob- 
servation; by  example,  to  attempt  to  indicate  how  clear  rela- 
tions may  be  established  between  clinical  and  laboratory  find- 
ings ;  to  illustrate  the  advantages  of  precise  methods  of  study ; 
to  ask  your  agreement  that  medicine  may  be  treated  as  an  exact 


Observations  Upon  Cardiac  Syncope  121 

science,  in  which  the  simple  facts  of  our  experience  may  be  ar- 
ranged and  sorted  out  into  the  compartments  of  cause  and  ef- 
fect, in  which  a  careful  and  deliberate  discrimination  between 
these  facts  and  hypotheses  may  play  a  prominent  and  appro- 
priate part  in  our  processes  of  thought ;  to  ask  your  support  for 
the  belief  that  the  proved  cause  of  a  clinical  symptom,  however 
rare  such  cause  may  be,  is  of  infinitely  greater  consequence  to 
us  than  a  hundred  plausible  suggestions  whose  validity  is  un- 
supported by  the  evidence  of  observation. 

REFERENCES 

Cohn  and  Lewis.     Heart,  1912-13,  IV,  7. 

Cohn  and  Lewis.     Heart,  1912-13,  IV,  15. 

Erlanger.     Journ.  exper.  Med.,  1905,  VII,  1. 

Erlanger   and   Blackmann.     Heart,   1909-10,   I,   177. 

Fredericq.     Arch,  intern,  d.  Physiol.,  1912,  XI,  405. 

Gossage.     Quart.  Journ.  of  Ned.,  1908-9,  II,  19. 

Hering.     Munch,  med.  Wochenschr.,  1912.,  No.  14  and  15. 

Hill.     Phil  Trans.  Roy.  Soc.,  1900,  B,  CXCIII,  69. 

Hoffmann.     Heart,  1912,  III,  213. 

Jex-Blake.     Brit.  med.  Journ.,  1913,  I,  425-492. 

Kussmaul  and  Tenner.     Xew  Sydenham  Society,  1859,  28  (trans.) 

Laslett.     Quart.  Journ.  of  Ned.,  1908-9,  II,  347. 

Levy.     Heart,  1912-13,  IV,  319  and  299. 

Lewis.     Heart,  1909-10,  I,  306. 

Lewis.     Heart,  1909-10,  I,  98. 

Lewis.     Journ.  exper.  Ned.,  1912,  XVI,  395. 

Lewis.     "Mechanism  of  the  Heart  Beat,"  1911,  188. 

Mackenzie  "Diseases  of  the  Heart/'  1913,  3rd  ed.,  Fig.  141. 

MacWilliam.     Brit.  med.  Journ.,  1889,  I,  6. 

Neubiirger  and  Edinger.     Berl  Uin,  Wochenschr.,  1898,  XXXV, 

69  and  100. 

Rihl.     Zeitschr.  f.  exper.  Pathol  u.  Therap.,  1905,  II,  83. 
Robinson.     Journ.  of  exper.  Med.,  1912,  XVI,  291. 
Schiff.     Lehrbuch  d.  Muskel  —  u.  NervenphysioL,  Lahr,  1858,  108. 
Webster.     Glasgow  med.  Rep.,  1901,  III,  413. 


INDEX 


Accelerated  heart  action,  116 

Acidosis,   81 

Adams-Stokes  syndrome,  46,  109 

Angina  sine  dolore,  102 

Asystole,  102 

Auricle : 

Origin  of  excitation  wave  in,  8 
Course  of  excitation  wave  in,  16 

Auricular  fibrillation,  46,  62,  119 

Auricular  flutter,  50,  119 

Auricular   sounds,   59 

Auriculo-systolic  murmur,   70 

A-V   bundle,    44,    106 

A-V  node,   44 

Bundle  branch   section,  26 
Bundle  of  His,  44,   106 


Digitalis,  45,  48,  51,   111 
Dilatation,   acute,   49,    102 
Diphasic  curve,  5 
Dyspnoea,  82 

Cardiac,  84 

Mechanical,  84,  89 

Nocturnal,  attacks  of,  85,  86 

Of  diabetes,  91 

Of  exercise,   91 

Of  exophthalmic  goitre,  92 

Of  high  altitude,  91 

Of  pneumonia,  91 

Of  pregnancy,   92 

Periodic,  94 

Relation  to  cyanosis,  82 

Special  type  of,   85 

"Ursemic,"  88,  93 


Cerebral  anaemia,  effects  of,  109 
Cheyne-Stokes  breathing,  86  . 
Chloroform,  death  under,   113 
Clinical     medicine    and    laboratory 

methods,  35,  53,  81 
Concentration  point,  21 
Coronary  arteries: 

Anastomoses,   115 

Plugging  of,  101,  115 

Da  Costa,  48 

Diabetes  and  breathlessness,  91 

Diastolic  Arrest,  102 


Early  diastolic  murmur,  73 
Electrocardiogram,  38 
Endocardial   leads,   27,    29 
Excitation  Wave: 

Conduction  rates,  19,  27,  30 

Course  in  auricle,   16 

Course  in  ventricle,  22 

Curve  form  governed  by  direction 
of,  6,  11 

General  principles  of  studying,  4 

Origin  in  auricle,  8 

Rate  of  travel,  19,  27,  30 

Reversal  of,  7 


123 


124 


Index 


Exercise  and  breathlessness,  91 
Extrasystoles : 

Auricular,  40 

Ventricular,  42 
Extrinsic  deflections,   12 

Fainting,  vasomotor,  101 
Favourable  leads,  8 
Fibrillation  of  auricles,  46,  62,  119 
Fibrillation  of  ventricles,   110 
Forced  beats,  11 

Gallop  rhythm,  61 
Graphic  records,  38,  99 

Heart-block,  44,  59,  66,  104,  107 
Heart-sound  recorder,  54 
Heart-sounds  and  murmurs,  53 
High  altitude  and  breathlessness,  91 

Intrinsic  deflections,   12,   13 
Isopotentiality,  7 

Laboratory    methods     and     clinical 

medicine,   35,   53,   81 
"  Lub-dup,"  59 

Mitral  stenosis,  67 

Murmurs  of  mitral  stenosis,  67 

Classification  of,  76 

During  fibrillation,  73 

During  heart-block,  71 


General  theory  of,  77 
Musical  murmurs,   56 

Pace-maker : 

Displacement  of,  43 

Situation  of,  8 
Periodic  breathlessness,  94 
Pig's  heart,  10 

Pneumonia  and  breathlessness,  91 
Presystolic  murmur,  70 

Disappearance  of,  73 
Primary  negativity,   9,    14 
Prolonged  Ag-Fg  interval,  61,  73 
Purkinje  distribution  of  excitation 
wave,  26,  30 

Relative  negativity,  5 

Section   of  bundle  branch,  26 
Sino-auricular  node,  10 
Standstill  of  heart,  103 
Standstill  of  ventricle,   104 
Syncope,  46,  97 

Timing  of  sounds,  56 
Tuning  fork,  54 

Unexpected  death,    101,    111,  etc. 

Veins,  course  of  excitation  wave  in, 

16,  17 
Ventricular  fibrillation,  110 


MEDICAL  MONOGRAPHS 

PUBLISHED  BY 

PAUL  B.  HOEBER 

67-69  EAST  sgth  St.,  NEW  YORK 

This  catalogue  comprises  only  our  own  publications.  It 
will  be  noticed  that  particular  care  has  been  exercised  in  the 
selection  of  Monographs  of  timely  interest. 

We  are  always  glad  to  consider  the  publication  of  new  and 
original  medical  works.  Correspondence  with  Authors  is  in- 
vited. 

ADAM — Asthma  and  Its  Radical  Treatment.  By  JAMES 
ADAM,  M.A.,  M.D.,  F.R.C.P.S.  Hamilton.  Dispensary  Aural 
Surgeon,  Glasgow  Royal  Infirmary.  8vo,  Cloth,  viii-fi84 
pages,  Illustrated  $1.50  net. 

ARMSTRONG— I.  K.  Therapy,  With  Special  Reference  to 
Tuberculosis.  By  W.  E.  M.  ARMSTRONG,  M.A.,  M.D. 
Dublin.  Bacteriologist  to  the  Central  London  Ophthalmic 
Hospital,  Late  Assistant  in  the  Inoculation  Department,  St. 
Mary's  Hospital,  Padding,  W. 
8vo,  Cloth,  x-f  93  pages,  Illustrated  $1.50  net. 

BEDDOES — Syphilis,  Its  Diagnosis,  Prognosis,  Preven- 
tion and  Treatment.  By  THOMAS  HUGH  BEDDOES,  M.B., 
B.C.  Camb.,  F.R.C.S.  Eng.  Surgeon  to  the  London  Hos- 
pital for  Diseases  of  the  Skin.  Surgeon  to  the  Westminster 
General  Dispensary.  Registrar,  London  Lock  Hospital ;  Fel- 
low of  the  Royal  Society  of  Medicine ;  Fellow  of  the  Trop- 
ical Society.  I2mo,  Cloth,  224  pages  $2.00  net. 

BIGG — Indigestion,  Constipation  and  Liver  Disorder.  By 
G.  SHERMAN  BIGG,  Fellow  of  the  Royal  College  of  Sur- 
geons ;  Fellow  of  the  Royal  Institute  of  Public  Health ;  Late 
Surgeon  Captain,  Army  Medical  Staff;  Surgeon  Allahabad 
India.  I2mo,  Cloth,  viii-f-i68  pages $1.50  net. 

BRUCE — Lectures  on  Tuberculosis  to  Nurses.     Based  on 
a  course  delivered  .to  the   Queen   Victoria  Jubilee   Nurses. 
By  OLLIVER  BRUCE,  M.R.C.S.,  L.R.C.P.,  Joint  Tuberculosis 
Officer,  County  of  Essex. 
i2mo,  Cloth,  134  pages.     Illustrated .$1.00  net. 

BRUNTON — Therapeutics    of    the    Circulation.     By     SIR 

LAUDER  BRUNTON,  M.D.,  D.Sc.,  LL.D.  Edin.,  LL.D.,  Aberd., 

F.R.C.P.,  F.R.S.     Consulting  physician  to  St.  Bartholomew's 

Hospital. 

Second   Edition,   entirely   revised.     Cloth,   xxiv-|-536  pages, 

no  illustrations $2.50  net. 


HOEBER'S  MEDICAL  MONOGRAPHS 

BULKLEY — Compendium  of  Diseases  of  the  Skin.  Based 
on  an  analysis  of  thirty  thousand  consecutive  cases.  With 
a  Therapeutic  Formulary,  by  L.  DUNCAN  BULKLEY,  A.M., 
M.D.  Physician  to  the  New  York  Skin  and  Cancer  Hos- 
pital; Consulting  Physician  to  the  New  York  Hospital. 
8vo,  Cloth,  xviii+286  pages  $2.00  net. 

BULKLEY— Cancer:    Its    Cause    and    Treatment.     By    L. 
DUNCAN  BULKLEY,  A.M.,  M.D. 
8vo,  Cloth,  224  pages $1.50  net. 

BULKLEY — Diet  and  Hygiene  in  Diseases  of  the  Skin. 
By  L.  DUNCAN  BULKLEY,  A.M.,  M.D. 
8vo,  Cloth,  xvi-j-194  pages $2.00  neb. 

BULKLEY — The  Influence  of  the  Menstrual  Function  on 
Certain  Diseases  of  the  Skin.  By  L.  DUNCAN  BULKLEY, 
A.M.,  M.D.  I2mo,  Cloth,  108  pages $1.50  net. 

BULKLEY — The  Relations  of  Diseases  of  the  Skin  to 
Internal  Disorders:  With  Observations  on  Diet,  Hygiene 
and  General  Therapeutics.  By  L.  DUNCAN  BULKLEY, 
A.M.,  M.D.  i2mo,  Cloth,  175  pages $1.50  net 

BULKLEY — Principles  and  Application  of  Local  Treat- 
ment in  Diseases  of  the  Skin.  By  L.  DUNCAN  BULKLEY, 
A.M.,  M.D.  i2mo,  Cloth,  130  pages  $1.50  net. 

CAUTLEY — The  Diseases  of  Infants  and  Children.     By 
EDMUND   CAUTLEY,   M.D.   Cantab.,   F.R.C.P.   Lond.     Senior 
Physician    to    the    Belgrave    Hospital    for    Children;    Phy- 
sician to  the  Metropolitan  Hospital;  etc. 
Large  8vo,  Cloth,   1042  pages    $7.00  net. 

COOPER — Pathological  Inebriety.  Its  Causation  and 
Treatment.  By  J.  W.  ASTLEY  COOPER.  Medical  Super- 
intendent and  Licensee  of  Ghyllwood  Sanatorium  near  Cock- 
ermouth,  Cumberland.  With  introduction  by  SIR  DAVID 
FERRIER,  M.D.,  F.R.S. 
I2mo,  Cloth,  xvi+i5i  pages  $1.50  net. 

COOPER — The    Sexual    Disabilities    of   Man,    and    Their 
Treatment.     By   ARTHUR   COOPER.     Consulting   Surgeon   to 
the  Westminster  General  Dispensary ;  Formerly  Surgeon  to 
the  Male  Lock  Hospital,  London. 
2nd  Edition,  I2mo,  Cloth,  viii-|-2O4  pages  $2.00  net. 

CORBETT-SMITH— The  Problem  of  the  Nations.  A 
Study  in  the  Causes,  Symptoms  and  Effects  of  Sexual  Dis- 
ease, and  the  Education  of  the  Individual  therein.  By  A. 
CORBETT-SMITH,  Editor  of  "The  Journal  of  State  Medicine" ; 
Lecturer  in  Public  Health  Law  at  the  Royal  Institute  of 
Public  Health.  Large  8vo,  Cloth,  xii-|-io7  pages.  .$1.00  net. 

CORNET— Acute      General      Miliary     Tuberculosis.    By 

PROFESSOR  DR.  G.  CORNET,  Berlin  and  Reichenhall.    Trans- 
lated by  F.  S.  TINKER,  B.A.,  M.B.,  etc. 
8vo,  Cloth,  viii+io7  pages $1.50  net. 


HOEBER'S  MEDICAL  MONOGRAPHS 

CROOKSHANK— Flatulence  and  Shock.     By  F.  G.  CROOK- 
SHANK,  M.D.,  Lond.,  M.  R.  C.  P.     Physician  (Out  Patients) 
Hampstead  General  and  N.  W.  Lond.  Hospital;  Assistant 
Physician  The  Belgrave  Hospital  for  Children  S.W. 
8vo,  Cloth,  iv-f-47  pages $1.00  net. 

EDRIDGE-GREEN — The  Hunterian  Lectures  on  Colour- 
Vision  and  Colour  Blindness.  Delivered  before  the 
Royal  College  of  Surgeons  of  England  on  February  1st,  and 
3rd,  1911.  By  Professor  F.  W.  EDRIDGE- GREEN,  M.D.  Durh., 
F.R.C.S.  England.  Beit  Medical  Research  Fellow. 
8vo,  Cloth,  x+76  pages  $1.50  net. 

EHRLICH — Experimental  Researches  on  Specific  Thera- 
peutics. By  PROF.  PAUL  EHRLICH,  M.D.,  D.Sc.  Oxon. 
Director  of  the  Konigliches  Institut  fur  Experimentelle 
Therapie,  Frankfort.  The  Harben  Lectures  for  1907  of  The 
Royal  Institute  of  Public  Health. 
i6mo,  Cloth,  x-f95  pages $1.00  net. 

EIN HORN— Lectures    on    Dietetics.     By    MAX    EINHORN, 
Professor    of    Medicine    at   the    New    York    Post-Graduate 
Medical  School  and  Hospital  and  Visiting  Physician  to  the 
German  Hospital,  New  York. 
I2mo,  Cloth,  xvi-j-156  pages $1.00  net. 

ELLIOT — Sclero-Corneal  Trephining  in  the  Operative 
Treatment  of  Glaucoma.  By  ROBERT  HENRY  ELLIOT,  M.D., 
B.S.  Lond.,  Sc.D.  Edin.,  F.R.C.S.  Eng.,  Etc.  Lieut.  Colonel 
I. M.S.  Second  Edition.  8vo,  Cloth,  135  pages,  33  illustra- 
tions   $3.00  net. 

EMERY — Immunity  and  Specific  Therapy.  By  WM. 
D'EsTE  EMERY,  M.D.,  B.Sc.  Lond.  Clinical  Pathologist  to 
King's  College  Hospital  and  Pathologist  to  the  Children's 
Hospital,  Paddington  Green ;  formerly  Assistant  Bacteriolo- 
gist to  the  Royal  College  of  Physicians  and  Surgeons,  and 
sometime  Lecturer  on  Pathology  and  Bacteriology  in  the 
University  of  Birmingham. 
8vo,  Cloth,  448  pages,  with  2  ills $3.50  net. 

ADOPTED   BY    THE    U.    S.    ARMY 

GILES — Anatomy  and  Physiology  of  the  Female  Genera- 
tive Organs  and  of  Pregnancy.  By  ARTHUR  E.  GILES, 
M.D.,  B.Sc.  Lond.  M.R.C.P.  Lond.;  F.R.C.S.  Ed.  Gynecolo- 
gist to  the  Prince  of  Wales  General  Hospital,  Tottenham, 
and  Surgeon  to  the  Chelsea  Hospital  for  Women. 
Large  8vo,  24  pages  with  manikin $1.50  net. 

GREEFF — Guide  to  the  Microscopic  Examination  of  the 
Eye.  By  PROFESSOR  R.  GREEFF.  Director  of  the  Uni- 
versity Ophthalmic  Clinique  in  the  Royal  Charity  Hospital, 
Berlin.  With  the  co-operation  of  PROFESSOR  STOCK  and  PRO- 

3 


HOEBER'S  MEDICAL  MONOGRAPHS 

FESSOR  WINTERSTEINER.     Translated  from  the  third  German 
Edition  by  HUGH-  WALKER,  M.D.,  M.B.,  CM.     Ophthalmic 
Surgeon  to  the  Victoria  Infirmary,  Glasgow. 
Large  8vo,  Cloth,  86  pages,  Illustrated  $2.00  net. 

HARRIS — Lectures  on  Medical  Electricity  to  Nurses.     An 

Illustrated  Manual  by  J.  DELPRATT  HARRIS,  M.D.  Durh., 
M.R.C.S.  Senior  Surgeon  and  Honorary  Medical  Officer 
in  charge  of  the  Electrical  Department,  Royal  Devon  Hosp. 
I2mo,  Cloth,  88  pages.  Illustrated  $1.00  net. 

HOFMANN-GARSON— Remedial  Gymnastics  for  Heart 
Affections.  Used  at  Bad-Nauheim.  Being  a  translation 
of  "Die  Gymnastik  der  Herzleidenden"  von  DR.  MED. 
JULIUS  HOFMANN  und  DR.  MED.  LUDVVIG  POHLMAN.  Berlin 
and  Bad-Nauheim.  By  JOHN  GEORGE  GARSON,  M.D.  Edin.t 
etc.  Physician  to  the  Sanatoria  and  Bad-Nauheim,  Evers- 
ley,  Hants.  With  51  full-page  illustrations  and  diagrams. 
Large  8vo,  Cloth,  xvi-)-i28  pages  $2.00  net. 

HOWARD — The   Therapeutic   Value   of   the   Potato.    By 

HEATON  C.  HOWARD,  L.R.C.P.  Lond.,  M.  R.  C.  S.  Eng.  8vo, 
paper,  vi-|-3i  pages,  Illustrated  500 

JELLETT — A   Short   Practice   of  Midwifery  for   Nurses. 

Embodying  the  treatment  adopted  in  the  Rotunda  Hospital, 
Dublin.  By  HENRY  JELLETT,  B.A.,  M.D.  (Dublin  Univer- 
sity) F.R.C.P.I.,  Master  Rotunda  Hospital;  Extern  Exam- 
iner in  Midwifery  and  Gynecology,  Victoria  University, 
Manchester ;  Late  King's  Professor  of  Midwifery ;  Univer- 
sity of  Dublin.  With  six  plates  and  169  illustrations  in  the 
text,  also  an  appendix,  a  glossary  of  Medical  Terms,  and 
the  Regulations  of  the  Central  Midwives  Board. 
I2mo,  Cloth,  xvi-f-5o8  pages  $2.50  net. 

KENWOOD— Public  Health  Laboratory  Work.  By 
HENRY  R.  KENWOOD,  M.B.,  F.R.S.  Edin.,  P.P.H.,  F.C.S., 
Chadwick.  Professor  of  Hygiene  and  Public  Health,  Uni- 
versity of  London;  Medical  Officer  of  Health  and  Public 
Analyst  for  the  Metropolitan  Borough  of  Stoke  Newington; 
Examiner  in  Public  Health  to  the  Royal  College  of  Phy- 
sicians and  Surgeons,  London,  etc. 
6th  Edition,  8vo,  Cloth,  418  pages.  Illustrated. ..  .$4.00  net. 

LEWERS — A  Practical  Textbook  of  the  Diseases  of 
Women.  By  ARTHUR  H.  N.  LEWERS,  M.D.  Lond.  Senior 
Obstetric  Physician  to  the  London  Hospital ;  Late  Exam- 
iner in  Obstetric  Medicine  at  the  University  of  London ; 
University  Scholar  &  Gold  Medallist  in  Obstetric  Medicine,. 
London  University,  etc.  With  258  illustrations,  13  colored 
plates,  5  plates  in  black  and  white. 
7th  Edition,  8vo,  Cloth,  xii-f-54O  pp $4.00  net^ 


HOEBER'S  MEDICAL  MONOGRAPHS 

LEWIS — Clinical  Disorders  of  the  Heart  Beat.  A  Hand- 
book for  practitioners  and  Students.  By  THOMAS  LEWIS, 
M.D.,  D.Sc.,  F.R.C.P.  Assistant  Physician  and  Lecturer  in 
Cardiac  Pathology,  University  College  Hospital,  Physician 
to  Out-Patients,  City  of  London  Hospital  for  Diseases  of 
the  Chest.  SECOND  EDITION. 
8vo,  Cloth,  1 16  pages.  Illustrated  $2.00  net. 

LEWIS — Lectures  on  the  Heart.  Comprising  the  Herter 
Lectures  (Baltimore),  a  Harvey  Lecture  (New  York)  and 
an  address  to  the  Faculty  of  Medicine  at  McGill  Univer- 
sity (Montreal),  by  THOMAS  LEWIS,  M.D.,  F.R.C.P.  Phy- 
sician, City  of  London  Hospital ;  Assistant  Physician  and 
Lecturer  in  Cardiac  Pathology,  University  College  Hos- 
pital, London.  With  83  illustrations $2.00  net. 

LEWIS — The  Mechanism  of  the  Heart  Beat.  With  spe- 
cial reference  to  its  Clinical  Pathology.  By  THOMAS  LEWIS, 
M.D.,  D.Sc.,  M.R.C.P.  Lecturer  in  Cardiac  Pathology,  Uni- 
versity College  Hospital  Medical  School;  Physician  to  Out- 
Patients,  City  of  London  Hospital  for  the  Diseases  of  the 
Chest.  Large  8vo,  Cloth,  295  pages,  227  Illus $7.00  net. 

McCLURE — A    Handbook    of    Fevers.     By    J.    CAMPBELL 
McCLURE,  M.D.,  Glasgow.     Physician  to  Out-Patients,  The 
French  Hospital,  and  Physician  to  the  Margaret  Street  Hos- 
pital for  Consumption  and  Diseases  of  the  Chest,  London. 
8vo,  Cloth,  470  pages,  with  charts  $3.50  net. 

McCRUDDEN — The   Chemistry,  Physiology  and  Pathol- 
ogy  of   Uric   Acid,   and   the    Physiologically    Important 
Purin   Bodies.     With    a    discussion    of   the    Metabolism    in 
Gout.     By  FRANCIS  H.  MCCRUDDEN, 
i2mo,  Paper.    318  pages  $2.00  net. 

McKISACK— Systematic-Case  Taking.     A   Practical  guide 
to    the    examination    and    recording    of    medical    cases.     By 
HENRY  LAWRENCE  McKisACK,  M.D.,  M.R.C.P.  Lond.     Phy- 
sician to  the  Royal  Victoria  Hospital,  Belfast. 
i2mo,  Cloth,  166  pages  $1.50  net. 

MACKENZIE — Symptoms   and   their   Interpretation.     By 

JAMES  MACKENZIE,  M.D.,  LL.D.,  Aber.  and  Edin.     Lecturer 

on  Cardiac  Research,  London  Hospital. 

8vo,  Cloth.     Illustrated.     xxii-f~3O4  pages   $3.00  nel\ 

MACMICHAEL— The  Gold-Headed  Cane.  By  WILLIAM 
MACMICHAEL.  Reprinted  from  the  2nd  Edition.  With  a 
Preface  by  SIR  WILLIAM  OSLER  and  an  Introduction  by  DR. 
FRANCIS  R.  PACKARD. 

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back,  and  gold  stamping  on  back  and  side  $3.00  net. 

5 


HOEBER'S  MEDICAL  MONOGRAPHS 

MARTINDALE     and    WESTCOTT— "Salvarsan"     "606" 
(Dioxy-Diamino    Arsenobenzol)    Its    Chemistry,    Phar- 
macy and  Therapeutics.     By  W.   HARRISON   MARTINDALE, 
Ph.D.  Marburg  F.C.S.,  and  W.  WYNN  WESTCOTT,  M.B. 
8vo,  Cloth,  xvi+76  pages $1.50  net. 

MINETT— Diagnosis    of    Bacteria    and    Blood    Parasites. 

By  E.  P.  MINETT,  M.D.,  D.P.H.,  D.T.M.  and  H.,  M.R.C.S., 
L.R.C.P.     Assistant  Government  Medical  Officer  of  Health 
and  Bacteriologist  British  Guiana. 
I2mo,   Cloth,   viii+8o  pages    $1.00   net. 

MOTT — Nature  and  Nurture  in  Mental  Development.  By 
F.  W.  MOTT,  M.D.,  F.R.S.,  F.R.C.P.  Pathologist  to  the 
London  County  Asylums,  Consulting1  physician  to  Charing 
Cross  Hospital  and  the  Queen  Alexandra  Military  Hospital. 
I2mo,  Cloth,  151  pages,  with  Diagrams $1.50  net. 

MURRELL — What    to    do    in    Cases    of    Poisoning.     By 

WILLIAM  MURRELL,  M.D.,  F.R.C.P.  Senior  Physician  to 
the  Westminster  Hospital ;  Lecturer  on  Clinical  Medicine 
and  joint  lecturer  on  the  principles  and  practice  of  medi- 
cine ;  Late  examiner  in  the  Universities  of  Edinburgh,  Glas- 
gow and  Aberdeen,  and  to  the  Royal  College  of  Physicians. 
Eleventh  Edition,  i6mo,  Cloth,  283  pages $1.00  net. 

OLIVER — Lead  Poisoning:  From  the  Industrial,  Med- 
ical and  Social  Point  of  View.  Lectures  delivered  at  the 
Royal  Institute  of  Public  Health.  By  SIR  THOMAS  OLIVER, 
M.A.,  M.D.,  F.R.C.P.  Consulting  Physician,  Royal  Victoria 
Infirmary,  and  Professor  of  the  Principles  and  Practice  of 
Medicine,  University  of  Durham  College  of  Medicine,  New- 
castle-upon-Tyne,  Late  Medical  Expert,  Dangerous  Trades 
Committee;  Home  Office. 
Large  I2ino,  Cloth,  294  pages $2.00  net. 

OSLER— Two  Essays.  By  SIR  WILLIAM  OSLER,  M.D. 
Regius  Professor  of  Medicine  at  Oxford. 

Vol.  i.  A  Way  of  Life.  An  Address  to  Yale  Students, 
Sunday  Evening,  April  2Oth,  1913.  i6mo,  Cloth,  61 
pages  5oc  net. 

Vol.  2.  Man's  Redemption  of  Man.  A  Lay  Sermon, 
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Cloth,  63  pages 5oc  net. 

The  set  neatly  bound  and  boxed  $1.00  net. 

(A  handsome  presentation  set.) 

OTT — Fever,  Its  Thermotaxis  and  Metabolism.  By  ISAAC 
OTT,  A.M.,  M.B.  Professor  of  Physiology  in  the  Medico- 
Chirurgical  College  of  Philadelphia;  Ex-Fellow  in  Biology 
Johns  Hopkins  University ;  Consulting  Neurologist,  Norris- 
town  Asylum,  Penna. ;  Ex- President  of  American  Neuro- 
logical Association,  Etc.,  I2mo,  Cloth,  168  pp.,  illus..$i.5o  net. 

6 


HOEBER'S  MEDICAL  MONOGRAPHS 

PAGET — For  and  Against  Experiments  on  Animals.  Evi- 
dence before  the  Royal  Commission  of  Vivisection.  By 
STEPHEN  PAGET,  F.R.C.S.  Hon.  Secretary  Research  De- 
fence Society.  With  an  introduction  by  THE  RIGHT  HON. 
THE  EARL  OF  CROMER,  O.M.,  G.C.M.G.,  G.C.B. 
8vo,  Cloth,  Illustrated,  xii-j-344  pages  $1.50  net. 

PEGLER — Map  Scheme  of  the  Sensory  Distribution  of  the 
Fifth  Nerve  (Trigeminus)  with  Its  Ganglia  and  Connec- 
tions. By  L.  HEMINGTON  PEGLER,  M.D.,  M.R.C.S.  Senior 
Surgeon,  Metropolitan  Ear,  Nose  and  Throat  Hospital,  Etc. 

Mounted  on  Rollers,  4  ft.  I  in.  x  4  ft.  8  in $7.00  net. 

Folded  in  Cloth  Binder $8.00  net. 

RAWLING — Landmarks  and  Surface  Markings  of  the  Hu- 
man Body.  By  L.  BATHE  RAWLING,  M.B.,  B.C.  (Cant) 
F.R.C.S.  (Lond.)  Surgeon  with  charge  of  Out-Patients, 
Late  Senior  Demonstrator  of  Anatomy  at  St.  Bartholomew's 
Hospital ;  Late  Assistant-Surgeon  to  the  German  Hospital, 
Dalston;  Late  Hunterian  Professor  Royal  College  of  Sur- 
geons, England,  Etc.  FIFTH  EDITION. 
8vo,  Cloth,  31  plates.  xii-(-96  pages  of  text $2.00  net. 

RITCHIE — Auricular  Flutter.  By  WILLIAM  THOMAS 
RITCHIE,  M.D.,  F.R.C.P.E.,  F.R.S.E.  Physician  to  the 
Royal  Infirmary ;  Lecturer  on  the  Practice  of  Medicine, 
School  of  Medicine  of  the  Royal  Colleges;  Lecturer  on 
Clinical  Medicine  in  the  University  of  Edinburgh.  Large 
8vo,  Cloth,  xii+144  pages,  21  plates,  107  illus $3.50  net. 

RUTHERFORD— The     Ileo-Caecal     Valve.    By     A.     H. 

RUTHERFORD,  M.D.     Edin. 

8vo,  Cloth,  63  pages  of  text,  23  full  page  plates,  3  of  which 

are  colored $2.25  net. 

SAALFELD — Lectures  on  Cosmetic  Treatment.  A  Man- 
ual for  Practitioners.  By  DR.  EDMUND  SAALFELD  of  Berlin. 
Translated  by  J.  F.  DALLY,  M.A.,  M.D.,  B.C.  Cantab., 
M.R.C.P.  Lond.  Physician  to  the  St.  Marylebone  General 
Dispensary.  With  an  introduction  and  notes  by  P.  S. 
ABRAHAM,  M.A.,  M.D.,  B.Sc.,  F.R.C.S.I.,  Surgeon  for,  and 
Lecturer  on,  Diseases  of  the  Skin,  West  London  Hospital 
and  College.  Late  Surgeon  to  the  Skin  Hospital  Blackfriars. 
I2mo,  Cloth,  xii-f  186  pages,  Illustrated  $i-75  net. 

SCOTT— The    Road   to   a   Healthy   Old   Age.     Essays   by 

THOMAS  BODLEY  SCOTT,  M.D.    i2mo,  Cloth,  104  pp...$i.oo  net. 

SENATOR  and  KAMINER— Marriage  and  Disease.  Be- 
ing an  Abridged  Edition  of  "Health  and  Disease  in  Rela- 
tion to  Marriage  and  the  Married  State."  By  PROFESSOR 
H.  SENATOR  and  DR.  S.  KAMINER.  Translated  from  the 
German  by  J.  DULBERG,  M.D. 
8vo,  Cloth,  452  pages $2.50  net. 


HOEBER'S  MEDICAL  MONOGRAPHS 

SMITH — Some  Common  Remedies,  and  Their  Use  in 
Practice.  By  EUSTACE  SMITH,  M.D.  Fellow  of  the  Royal 
College  of  Physicians ;  Senior  Physician  to  the  East  Lon- 
don Hospital  for  Children ;  Consulting  Physician  to  the 
Victoria  Park  Hospital  for  Diseases  of  the  Chest. 
8vo,  Cloth,  viii-|-ii2  pages $1.25  net. 

SQUIER  and   BUGBEE— Manual   of  Cystoscopy.     By  J. 
BENTLY   SQUIER,    M.D.     Professor   of   Genito-Urinary    Sur- 
gery,  New  York   Post-Graduate   Medical   School  and  Hos- 
pital, and  HENRY  G.  BUGBEE,  M.D. 
8vo,  Flex.  Leather,  xiv-(-ii7  pp.,  26  colored  plates. $3.00  net. 

ADOPTED  BY  THE  U.   S.  ARMY 

STARK — The  Growth  and  Development  of  the  Baby.    A 

tabular  chart,  giving  the  result  of  personal  observation, 
verified  by  authoritative  data,  as  to  development,  weight, 
height,  etc.,  during  the  first  seven  years.  By  MORRIS 
STARK,  M.A.,  B.S.,  M.D.  Instructor  of  Pediatrics,  New 
York  Post  Graduate  Medical  School,  etc. 
Heavy  paper,  20  by  25  inches  5oc  net. 

STEPHENSON — Eye-Strain   in   Every-day   Practice.     By 

SIDNEY     STEPHENSON,     M.B.,     C.M.     Edin.,     D.O.     Oxon, 
F.R.C.S.   Edin.     Ophthalmic   Surgeon  to  the  Queen's   Hos- 
pital for  Children ;  Editor  of  the  Ophthalmoscope. 
8vo,  Cloth,  x+i39  pages $1.50  net. 

STEPHENSON— A  Review  of  Hormone  Therapy.     1913 

8vo,  Cloth,  viii-f-!7O  pages $1.00  net. 

Bound   and    interleaved    edition    of   the    famous    "Hormone 
Number"  of  the  "Prescriber"  (Edinburgh). 

SWIETOCHOWSKI— Mechano-Therapeutics    in    General 
Practice.     By  G.  DE  SWIETOCHOWSKI,  M.D.,  M.R.C.S.     Fel- 
low of  the  Royal   Society  of  Medicine;   Clinical  Assistant, 
Electrical  and  Massage  Department  King's  College  Hosp. 
I2tno,  Cloth,  xiv+i4i  pp.,  31  Illustrations  $1.50  net 

TURNER  and  PORTER— The  Skiagraphy  of  the  Acces- 
sory Nasal  Sinuses.  By  A.  LOGAN  TURNER,  M.D., 
F.R.C.S.E.,  F.R.S.E.  Surgeon  to  the  Ear  and  Throat  De- 
partment, The  Royal  Infirmary,  Edinburgh,  and  W.  G. 
PORTER,  M.B.,  B.Sc.,  F.R.C.S.E.  Surgeon  to  the  Eye  and 
Throat  Infirmary,  Edinburgh. 
Quarto,  Cloth, '45  pages  of  text.  39  plates $4.50  net. 

WANKLYN— How  to  Diagnose  Smallpox.  A  Guide  for 
General  Practitioners,  Post-Graduate  Students  and  Others. 
By  W.  McC  WANKLY'N,  B.A.,  Cantab.,  M.R.C.S.,  L.R.C.P., 
D.P.H.  Assistant  Medical  Officer  of  the  London  County 
Council  and  formerly  Medical  Superintendent  of  the  River 
Ambulance  Service  (Small-pox). 
8vo,  Cloth,  102  pages.  Illustrated $1.50  net. 


HOEBER'S  MEDICAL  MONOGRAPHS 

WHITE — The     Pathology     of     Growth.      Tumours.      By 

CHARLES  POWELL  WHITE,  M.C,  F.R.C.S.     Director,  Pilking- 
ton   Cancer   Research   Fund,   Pathologist   Christie   Hospital, 
Special  Lecturer  in  Pathology,  University  of  Manchester. 
Svo,  Cioth,  xvi+235  pages.     Illustrated  $3.50  net. 

WATSON — Gonorrhoea  and  its  Complications  in  the 
Male  and  Female.  By  DAVID  WATSON,  M.B.,  C.M.,  Sur- 
geon Glasgow  Lock  Hospital,  Dispensary  Surgeon  for  Ve- 
nereal Diseases  Glasgow  Royal  Infirmary,  etc.,  etc. 
Svo,  Cloth,  375  pages,  72  illustrations,  12  plates,  some  col- 
ored   $3-75  net. 

WICKHAM  and  DEGRAIS— Radium.  As  employed  in 
the  treatment  of  Cancer,  Angiomata,  Keloids,  Local  Tuber- 
culosis and  other  affections.  By  Louis  WICKHAM,  M.V.O. 
Medecin  de  St.  Lazare ;  Ex-Chef  de  Clinique  a  L'Hopital 
St.  Louis,  and  PAUL  DEGRAIS,  Ex-Chef  de  Laboratoire  a 
L'Hopital  St.  Louis.  Chefs  de  service  au  Laboratoire 
Biologique  du  Radium;  Laureats  de  L' Academic  de  Medi- 
cine. 
Svo,  Cloth,  53  illustrations,  viii-f-m  pp $1.25  net. 

WRENCH— The     Healthy     Marriage.     A     Medical     and 
Psychological  Guide  for  Wives.     By  G.  T.  WRENCH,  M.D., 
B.S.     Lond.     Past  Assistant   Master  of  the  Rotunda  Hos- 
pital, Dublin. 
Svo,  Cloth,  x-j-300  pages   $1.50  net. 

WRIGHT — The  Unexpurgated  Case  against  Woman 
Suffrage.  By  SIR  ALMROTH  E.  WRIGHT,  M.D.,  F.R.S. 
Svo,  Cloth,  xii-f-i88  pages  $1.00  net. 

WRIGHT — On  Pharmaco-Therapy  and  Preventive  In- 
oculation; Applied  to  Pneumonia  in  the  African  Native 
with  a  discourse  on  the  Logical  Methods  which  ought  to  be 
Employed  in  the  Evaluation  of  Therapeutic  Agents.  By 
SIR  ALMROTH  E.  WRIGHT,  M.D.,  F.R.S. 
Svo,  Cloth,  124  pages  $i-75  net. 

Complete  catalogue  and  descriptive  circulars  will  be  sent  on 
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DATE    DUE    SLIP 

UNIVERSITY  OF  CALIFORNIA  MEDICAL  SCHOOL  LIBRARY 


THIS  BOOK  IS  DUE   ON  THE  LAST  DATE 
STAMPED  BELOW 


•&.  I 

<?Uv  Cuo 


MA.*.   - 

APR  1  8  1929 

NOv   i  , 
MAY  2  2  1930 
SEP  2  1  1931 


22  14)32 


1925 


1 


3  3  1832 

1934 

> 

SEP  12  1939 


1  0 

NOV  1  5  J946 


2?n-12,'19 


MEMCAL 

LIIBMAMY 


Villiam  "Vatt  Eerr 
Memorial 


University  of  California  Medical  School  Library 


